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Normotensive
Terms modified by Normotensive Selected AbstractsCOMPARATIVE EFFECTS OF TRAMADOL ON VASCULAR REACTIVITY IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2008Juliana M Raimundo SUMMARY 1The aim of the present study was to determine the effects of tramadol on vascular reactivity in aortic rings from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 2Aortic rings, with or without endothelium, were obtained from male WKY rats and SHR (15,20 weeks old) and prepared for isometric tension recording. Aortic rings were precontracted with phenylephrine (10 µmol/L) or 40 mmol/L KCl and then exposed to cumulative concentrations of tramadol (0.1,1 mmol/L). 3Tramadol produced a concentration-dependent relaxation of precontracted aortic rings from WKY rats and SHR, which was not dependent on functional endothelium. Vascular relaxation was significantly greater in rings from SHR than WKY rats. 4The concentration of tramadol necessary to produce a 50% reduction of the maximal contraction to phenylephrine (IC50) in rings with and without endothelium from SHR was 0.47 ± 0.08 and 0.44 ± 0.03 mmol/L, respectively (P = 0.76). 5Tramadol attenuated the contracture elicited by Ca2+ in depolarized tissue, suggesting that it may inhibit L-type Ca2+ channels. However, pretreatment with nicardipine (1 µmol/L) prevented the relaxation induced by tramadol in aortic rings from WKY rats and partially reduced its inhibitory effect in aortic rings from SHR. 6Pretreatment of endothelium-denuded aorta with glybenclamide (3 µmol/L), 4-aminopyridine (3 mmol/L), tetraethylammonium (3 mmol/L) and naloxone (100 µmol/L) did not affect tramadol-induced vasodilation of aortic rings from either WKY rats or SHR. 7Intravenous administration of tramadol (10 mg/kg) to conscious SHR significantly reduced both systolic and diastolic blood pressure from 171.4 ± 5.3 to 129.3 ± 5.3 (P = 0.002) and from 125.0 ± 6.5 to 57.8 ± 8.9 mmHg (P = 0.003), respectively. [source] HYPERHOMOCYSTEINAEMIA AND MEMBRANE FLUIDITY OF RED BLOOD CELLS IN NORMOTENSIVE AND HYPERTENSIVE MEN: AN ELECTRON PARAMAGNETIC RESONANCE INVESTIGATIONCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2007Kazushi Tsuda SUMMARY 1The purpose of the present study was to assess the possible link between plasma homocysteine and membrane fluidity in normotensive and hypertensive men. 2The membrane fluidity (a reciprocal value of membrane microviscosity) of red blood cells (RBC) was measured using an electron paramagnetic resonance and spin-labelling method. The membrane fluidity of RBC was decreased in hypertensive compared with normotensive men. 3Total plasma homocysteine levels were significantly higher in hypertensive men than normotensive men. In contrast, plasma levels of nitric oxide (NO) metabolites were significantly lower in hypertensive men than in normotensive men. The decreased membrane fluidity of RBC was associated with hyperhomocysteinaemia and reduced plasma levels of NO metabolites. 4The results of the present study suggest that hyperhomocysteinaemia may have a role in modulating the rheological behaviour of RBC and microcirculation in men by, at least in part, reducing NO bioavailability. [source] The haemodynamic response to propranolol in cirrhosis with arterial hypertension: a comparative analysis with normotensive cirrhotic patientsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010P. Sharma Aliment Pharmacol Ther 2010; 32: 105,112 Summary Background, Cirrhosis with arterial hypertension is not uncommon. Haemodynamic alterations in these patients and the effects of beta-blocker on hepatic venous pressure gradient (HVPG) and systemic haemodynamics have not been evaluated. Aims, To compare the systemic haemodynamic alterations in hypertensive and normotensive cirrhotics, and to investigate the effects of propranolol on these parameters. Methods, A retrospective analysis of consecutive hypertensive cirrhotic patients (n = 33) who underwent haemodynamic assessment and paired HVPG measurement was done. Normotensive cirrhotics (n = 50) served as controls. Results, Hypertensive patients had a significantly higher heart rate, systemic (SVRI), and pulmonary vascular resistance. There was a significant reduction in mean arterial pressure (MAP) in the hypertensive cirrhotic group from 112 (107,130) mmHg to 95 (77,114) mmHg (P < 0.01), but no change in the normotensives. SVRI remained the same in the hypertensive cirrhotic group, but it increased in the normotensives. There was no correlation between MAP reduction and HVPG reduction. Conclusions, The frequency of HVPG response with propranolol treatment in hypertensive cirrhotics is similar to normotensive cirrhotics. Propranolol treatment reduces MAP significantly in hypertensive patients with cirrhosis. Treatment with a nonselective beta-blocker is a good strategy for hypertensive cirrhotic patients. [source] Losartan modifies glomerular hyperfiltration and insulin sensitivity in type 1 diabetesDIABETES OBESITY & METABOLISM, Issue 6 2001S. Nielsen Aim: The effect of the angiotensin II receptor antagonist losartan on renal haemodynamics and insulin-mediated glucose disposal was examined in normotensive, normoalbuminuric type 1 diabetic patients using a double-blind, placebo-controlled, cross-over design. Methods: Diurnal blood pressure, glomerular filtration rate (GFR, determined using [125I]-iothalamate), renal plasma flow (RPF, determined using [131I]-hippuran) and urinary albumin excretion rate (UAE) were measured, and a hyperinsulinaemic, euglycaemic clamp with indirect calorimetry was performed in nine patients (age 30 ± 7 years (mean ±,s.d.), HbA1c 8.1 ± 1.1%) following 6 weeks' administration of either losartan 50 mg/day or placebo. Results: Diurnal blood pressure was significantly reduced after losartan compared with placebo (122/70 ± 11/8 vs. 130/76 ± 12/6 mmHg, p <,0.05). A significant decline in GFR (133 ± 23 vs. 140 ± 22 ml/min, p < 0.05) and filtration fraction (FF; GFR/RPF) (24.6 ± 3.5 vs. 26.2 ± 3.6%, p <,0.05) was observed in the losartan vs. placebo groups. RPF and UAE did not change. Isotopically determined glucose disposal rates were similar after losartan and placebo in the basal (2.61 ± 0.53 vs. 2.98 ± 0.93 mg/kg/min) and insulin-stimulated states (6.84 ± 2.52 vs. 6.97 ± 3.11 mg/kg/min). However, the glucose oxidation rate increased significantly after losartan vs. placebo in the basal state (1.72 ± 0.34 vs. 1.33 ± 0.18, mg/kg/min, p <,0.01) and during insulin stimulation (2.89 ± 0.75 vs. 2.40 ± 0.62 mg/kg/min, p <,0.03). Basal and insulin-stimulated non-oxidative glucose disposal tended to decrease after losartan; however, this was not significant. Endogenous glucose production and lipid oxidation were unchanged after treatment and similarly suppressed during hyperinsulinaemia. Glycaemic control, total cholesterol, high-density lipoprotein (HDL)-cholesterol and triglycerides were stable in both losartan and placebo groups. Conclusions: Losartan reduces blood pressure, glomerular hyperfiltration and FF, and improves basal and insulin-stimulated glucose oxidation in normotensive, normoalbuminuric type 1 diabetic patients. [source] QT interval prolongation in association with impaired circadian variation of blood pressure and heart rate in adolescents with Type 1 diabetesDIABETIC MEDICINE, Issue 11 2007K. Karavanaki Abstract Aims, The aim of our study was to assess diurnal blood pressure (BP) and heart rate variability and their possible relationship to the duration of the QT interval in adolescents with Type 1 diabetes. Methods, In 48 normotensive, normoalbuminuric diabetic adolescents, with a mean (± sd) age of 17.3 (± 4.1) years and a mean (± sd) diabetes duration of 8.5 (± 3.3) years, 24-h ambulatory BP was recorded. In addition, 24-h heart rate (HR) monitoring was performed and QT and corrected QT (QTc) intervals were estimated as indices of autonomic function. The patients were divided into two groups according to the absence of a decrease (non-dippers) or the presence of a decrease (dippers) in nocturnal diastolic BP (DBP). Results, In comparison with the dippers, the non-dippers showed reduced mean 24-h HR (79.6 vs. 84.0 beats/min, P = 0.05) and reduced mean daytime HR (81.3 vs. 86.0 beats/min, P = 0.05). The QT interval was prolonged in the non-dippers (366.3 vs. 347.5 ms, P = 0.015), and end systolic (28.7 vs. 25.9 mm, P = 0.004) and end diastolic left ventricular diameters (47.8 vs. 45.5 mm, P = 0.037) were greater. In stepwise multiple regression, HR variables were the most important factors affecting DBP ratio or the duration of the QT interval. Conclusions, In conclusion, normotensive diabetic adolescents with impaired nocturnal BP reduction also have impaired autonomic function tests, in association with prolonged QT interval and increased left ventricular diameters. These findings suggest that diabetic adolescents who have the ,non-dipper' phenomenon may need close follow-up for the possible development of vascular complications, such as cardiac arrhythmias and left-ventricular hypertrophy. [source] Pregnancy-induced sympathetic overactivity: a precursor of preeclampsia,EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2004T. Fischer Abstract Background, Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. Materials and methods, Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 ± 4, M2: 33 ± 5 weeks) and once postpartum (M3: 26 ± 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. Results, At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 ± 9, M2: 29 ± 14, M3: 9 ± 5 bursts min,1; P < 0·05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 ± 9, M2: 15 ± 7, M3: 16 ± 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 ± 5, M2: 27 ± 6, M3: 7 ± 4 bursts min,1; without preeclampsia (n = 16): M1: 21 ± 11, M2: 30 ± 16, M3: 9 ± 6 bursts min,1; P = NS]. Conclusion, Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail. [source] Short-term cortisol infusion in the brachial artery, with and without inhibiting 11,-hydroxysteroid dehydrogenase, does not alter forearm vascular resistance in normotensive and hypertensive subjectsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2002S. H. M. Van Uum Abstract Background Vascular tone is increased in primary hypertension, and glucocorticoids affect vascular tone. Local cortisol availability is modulated by activity of 11,-hydroxysteroid dehydrogenase (11,-HSD). As this activity may be decreased in patients with primary hypertension, vascular sensitivity to cortisol may be increased in these patients. We studied the acute effect of cortisol on forearm vascular resistance (FVR) by infusing cortisol directly into the brachial artery, both with and without inhibition of 11,-HSD, in normotensive and hypertensive subjects. Design Twenty normotensive volunteers and 20 patients with primary hypertension participated in the study. After a 10-min infusion of vehicle (glucose 5%), cortisol was infused into the brachial artery in three stepwise increasing doses (3·5, 10·5 and 35 µg per 100 mL of forearm volume), each for 10 min. Next, the participants received placebo or 500 mg glycyrrhetinic acid (GA) orally, and 150 min later the same infusion schedule was repeated. Forearm vascular resistance was measured during the last 5 min of the infused vehicle and of each dose. Arterial and forearm venous plasma samples for measurement of cortisol and cortisone were taken at the end of the infusions of glucose 5% and the highest cortisol dose. Results In both normotensive and hypertensive subjects, neither the infusion of cortisol nor the administration of GA changed FVR. Also 2 h after the cortisol infusion there remained no change in FVR in both the normotensive and hypertensive groups who received placebo. Following the infusion of the highest cortisol dose, total plasma cortisone levels in the venous plasma were decreased compared with levels in the arterial plasma (36 ± 3 and 49 ± 4 nmol L,1, respectively, P < 0·05). The protein-bound venous cortisone was 37·1 ± 4·8 nmol L,1 during the vehicle compared with 23·9 ± 3·7 nmol L,1 during the cortisol infusion (P < 0·01), whereas the free cortisone level was not altered by the cortisol infusion. Conclusions In both normotensive and hypertensive subjects, high-dose cortisol infusion both with and without 11,-HSD inhibition did not change FVR either immediately or after 2 h. We could not demonstrate in vivo 11,-HSD activity in the forearm vascular tissues. When binding of cortisone to CBG is changed, e.g. during cortisol infusion, arterio-venous changes in cortisone cannot reliably be used to assess (alterations in) local 11,-HSD activity. [source] Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activityEXPERIMENTAL PHYSIOLOGY, Issue 9 2010Jasenka Zubcevic GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitiude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart,brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABAA receptor-mediated neurotransmission in the NTS with gabazine (a specific GABAA receptor antagonist) at two levels of perfusion pressure (low PP, 60,70 mmHg; and high PP, 105,125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (,HR at low PP, ,57 ± 9 beats min,1; at high PP, ,177 ± 9 beats min,1; P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (,HR at low PP, ,45 ± 10 beats min,1; at high PP, ,58 ± 7 beats min,1). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (,,tSNA =,18.7 ± 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (,,tSNA = 23.7 ± 2.9%) and hypertensive rats (,,tSNA = 44.2 ± 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (,,tSNA =,25.2 ± 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, ,,tSNA =,29.4 ± 4.4%; high PP, ,tSNA =,22.8 ± 3%), whereas in the normotensive rat this was only significant at high PP (,,tSNA =,42.5 ± 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABAA receptor-mediated control of HR, it appears that GABAA receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity. [source] The PFA-100Ô system for the assessment of platelet function in normotensive and hypertensive pregnanciesINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 2 2001Marco Marietta Platelet function was studied in 30 pregnant women: 14 normotensive (C), and 16 affected by pregnancy-induced hypertension (PIH). Platelet aggregometry (PA) on platelet-rich plasma according to Born was compared with the new PFA-100Ô System (Dade International Inc, Miami, USA). This device evaluates platelet function (expressed in seconds as closure time, CT) in anticoagulated whole blood ex vivo at high shear rates. PA (expressed as percentage of light transmission) and CT were measured at baseline and after incubation with L-Arginine (L-Arg). MANOVA for repeated measures showed that L-Arg incubation significantly decreased PA (F=7.2, P < 0.05) and increased CT (F=6.05, P < 0.05) in the whole population of pregnant women. Moreover, we analysed separately both parameters in C and in PIH subjects. No differences in PA were found in both groups, neither at baseline nor after L-Arginine incubation. In contrast, CT was significantly longer in PIH in comparison to C before (95.9 s vs. 84 s, P < 0.05) as well after (115 s vs. 92 s, P < 0.05) L-Arginine incubation. Data from PFA-100Ô confirm our previous reports that during pregnancy the L-Arginine: Nitric Oxide pathway regulates platelet function. In hypertensive patients a significant decrease in platelet function was found by using the PFA-100Ô system. [source] Laparoscopic adrenalectomy for functioning and non-functioning adrenal tumors: Analysis of surgical aspects based on histological typesINTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2005JA H KU Background: The aim of this study was to evaluate whether hormonal functions of the tumor influence the operative results of laparoscopic adrenalectomy, and to analyse the clinical outcomes in patients with various hormonally active adrenal tumors. Methods: Clinical and pathological records of 68 patients were reviewed. The average age of patients was 40 years (range 20,75); 39 were women and 29 men. For the comparison, patients were divided into the non-functioning tumor group (n = 22) and the functioning tumor group (n = 46). Results: All laparoscopic adrenalectomies were finished successfully, and no open surgery was necessary. The median operative time and blood loss in the two groups were similar; however, in subgroup analysis, operative time for pheochromocytoma was significantly longer than that for non-functioning tumor (P = 0.044). No difference was noted in intra- and postoperative data between the groups. Of the 22 patients with aldosteronoma, 18 (81.8%) became normotensive and no longer required postoperative blood pressure medications. Adrenalectomy led to an overall reduction in the median number of antihypertensive medications (P < 0.001). All patients with Cushing adenoma had resolution or improvement of the signs and symptoms during follow-up periods. There was no evidence of biochemical or clinical recurrence in any patient with pheochromocytoma. Conclusion: The results of this retrospective review document that laparoscopic adrenalectomy is a safe and effective treatment for functioning as well as non-functioning adrenal tumors, although endocrinologic features may play a significant role. [source] Influence of hypertension on lower urinary tract symptoms in benign prostatic hyperplasiaINTERNATIONAL JOURNAL OF UROLOGY, Issue 11 2003KIMIO SUGAYA Abstract Aim:, To clarify the influence of hypertension on lower urinary tract symptoms (LUTS) we examined the relationship between blood pressure, LUTS, and the effect of terazosin on LUTS in patients with benign prostatic hyperplasia (BPH). Methods:, The subjects were patients who had LUTS and BPH. They were treated with terazosin (1 mg, twice-a-day) for 12 weeks. Calculation of the International Prostate Symptom Score (IPSS), measurement of blood pressure, and uroflowmetry were performed before and after 12 weeks of therapy. Patients were divided into a normotensive (NT) group and a hypertensive (HT) group at the time of first examination. Results:, The IPSS for urinary frequency and nocturia in BPH-HT patients (n = 21; mean age, 71 years) were significantly higher than those in the BPH-NT patients (n = 21; mean age, 69 years) before the administration of terazosin. The total IPSS the BPH-HT patients was also significantly higher than that of the BPH-NT patients. There were no differences of uroflowmetric parameters between the two groups. After 12 weeks of therapy, systolic and diastolic blood pressure decreased in the BPH-HT patients, but not in the BPH-NT patients. However, the systolic pressure of the BPH-HT patients was still significantly higher than that of the BPH-NT patients. The score for each IPSS parameter decreased in both groups, but the difference of the score between the two groups increased. Conclusion:, Hypertension may worsen LUTS and may decrease the improvement of symptoms by terazosin. [source] Incidentally discovered pheochromocytoma in long-term hemodialysis patientsINTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2002MASAAKI MORIOKA Abstract Two cases of pheochromocytoma incidentally discovered in long-term hemodialysis patients are reported. Case 1 was a 47-year-old-man who had been receiving hemodialysis for 18 years. Case 2 was a 33-year-old woman who had been receiving hemodialysis for 12 years. Both cases were normotensive, and no specific symptoms suggesting pheochromocytoma were seen. Plasma norepinephrine (NE) levels were not elevated in both cases; however, the level of epinephrine (E) was double the normal range in Case 2. After surgery, plasma E level returned to the normal range in Case 2; however, the level of NE remained almost the same as the preoperative value in both cases. Plasma catecolamine levels in long-term hemodialysis patients with pheochromocytoma are reviewed in the present report, and the efficacy of imaging methods in the diagnosis of pheochromocytoma are discussed. [source] An insulin-resistant hypertriglyceridaemic normotensive obese dog model: assessment of insulin resistance by the euglycaemic hyperinsulinaemic clamp in combination with the stable isotope techniqueJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 3-4 2003E. Bailhache Summary Many studies have shown that in humans insulin resistance (IR) is associated with obesity and hypertriglyceridaemia. The aim of our study was to develop slowly dietary-induced obesity in dogs through long-term overfeeding of a high-fat diet, and to characterize this IR, hypertriglyceridaemic and normotensive model. Insulin resistance was assessed by the euglycaemic hyperinsulinaemic clamp technique. The contribution of hepatic glucose production during the clamp was evaluated using a constant stable-isotope-labelled glucose infusion. Overfeeding a high-fat diet for 7 months was associated with a 43 ± 5% body weight increase. Insulin resistance was characterized by hyperinsulinaemia in the unfed state (10 ± 1 vs. 24 ± 1 ,U/ml, in healthy and obese dogs, respectively, p < 0.02) and by a reduction of the insulin-mediated glucose uptake (28 ± 3 vs. 16 ± 1 mg/kg/min, p < 0.02). Hepatic glucose production suppression under insulin infusion allowed to conclude that this reduced glucose uptake resulted from a decrease of insulin sensitivity in obese dogs. Furthermore, animals remained normotensive and exhibited a marked hypertriglyceridaemia (0.26 ± 0.04 vs. 0.76 ± 0.15 mmol/l, in healthy and obese dogs, respectively, p < 0.02). Because hypertriglyceridaemia is the most common lipid abnormality in insulin-resistant humans, this dog with slowly induced obesity may constitute a good model to study the consequences of IR in lipid metabolism independently of vascular changes. [source] New Considerations Relating to Class Effect With Angiotensin-Converting Enzyme Inhibitors-The PEACE StudyJOURNAL OF CLINICAL HYPERTENSION, Issue 3 2005Domenic A. Sica MD Angiotensin-converting enzyme inhibitor therapy provides positive outcome benefits in a number of cardiac scenarios including congestive heart failure, postmyocardial infarction, as well as in the hypertensive patient at cardiac risk. This benefit exists both in normotensive and hypertensive individuals and is present in those with various grades of cardiovascular risk. This beneficial cardiovascular effect has now been observed with several angiotensin-converting enzyme inhibitors, suggesting a class effect. The Prevention of Events with Angiotensin-Converting Enzyme Inhibition trial studied the effect of adding the angiotensinconverting enzyme inhibitor trandolapril to a contemporary therapeutic regimen of patients with stable coronary artery disease and preserved left ventricular function. In this study, the addition of trandolapril did not confer any additional benefit in terms of reducing the incidence of cardiovascular death, myocardial infarction, or coronary revascularization. The neutral findings in this trial add a new wrinkle to the concept of class effect for cardiovascular protection with angiotensin-converting enzyme inhibitors in patients with coronary artery disease. [source] Vascular endothelial growth factor, fms-like tyrosine kinase-1 (Flt-1) and soluble Flt-1 gene expressions in Korean pre-eclamptic placentasJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2010Jong-Sik Park Abstract Aim:, To assess the expressions of vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (Flt-1), and soluble Flt-1 (sFlt-1) genes in healthy normotensive and pre-eclamptic placentas of Korean women. Methods:, We investigated 12 healthy normotensive pregnant women and 10 pre-eclamptic pregnant women at Eulji University Hospital. The obtained placental tissues were analyzed using reverse transcription polymerase chain reaction and real-time quantitative polymerase chain reaction. Results:, The sFlt-1 messenger ribonucleic acid (mRNA) level was elevated 2.6 times more in pre-eclamptic placentas than in normal control placentas. However, the VEGF mRNA level of pre-eclamptic placentas was decreased. There was no difference in the Flt-1 mRNA level between control and pre-eclamptic placentas. Conclusions:, Our study showed that expressions of genes relating to angiogenesis were altered in Korean pre-eclamptic placentas. These results suggest that the alteration in expressions of sFlt-1 and VEGF genes might be associated with the pathogenesis of pre-eclampsia. [source] Responsiveness, affinity constants and receptor reserves for serotonin on aortae of aged normotensive and hypertensive ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2001Sheila A. Doggrell We have previously shown that the potency and affinity constants (KA values) for serotonin (5-HT) are greater, and the 5-HT2A -receptor reserve is lesser, on the aorta of 6-month-old spontaneously hypertensive rats (SHRs) compared with age-matched Wistar Kyoto normotensive (WKY) rats. The present study was undertaken to investigate whether these parameters are altered on the aorta with ageing and as hypertension progresses to heart failure. The effects of phenoxybenzamine on the serotonergic responses of the aortae of 24-month-old WKY rats and SHRs were determined. On WKY rat aorta, ageing from 6 to 24 months was associated with an increase in sensitivity and affinity for serotonin, and a loss of 5-HT2A -receptor reserve. On SHR aorta, ageing from 6 to 24 months was also associated with an increase in sensitivity and affinity for serotonin, but a loss of 5-HT2A -receptor reserve. The sensitivity to serotonin was greater on the 24-month-old SHR aorta (pD2 6.53) than age-matched WKY rat aorta (pD2 5.89). On the aorta of the 24-month-old WKY rats, the KA value for serotonin was 4.5 times 10,6 M, and the receptor occupancies required for 20 and 50% maximum responses were 12 and 29%, respectively. There was a similar affinity, but greater receptor reserves, for serotonin on the aorta of age-matched SHRs. In summary, we have shown changes in sensitivity, affinity and 5-HT2A -receptor reserves for serotonin on the aorta with ageing and in hypertension/heart failure. [source] Effects of Alcohol Withdrawal on 24 Hour Ambulatory Blood Pressure Among Alcohol-Dependent PatientsALCOHOLISM, Issue 12 2003Ramón Estruch Background: Although epidemiologic studies have reported an association between alcohol intake and high blood pressure (BP), the results of intervention studies have shown inconsistent results. We embarked on a study to determine whether different subgroups of alcohol-dependent patients may be identified in relation to the effect of alcohol on BP. Methods: Fifty alcohol-dependent men (mean age, 41.4 years) received 0.4 g of ethanol per kilogram of body weight every 4 hr in 200 ml of orange juice during 24 hr and the same amount of orange juice without ethanol during another 24 hr. Twenty-four hour ambulatory BP monitoring was performed during ethanol and orange juice intakes, as was hormonal and biochemical analysis. Results: Thirty-five (75%) alcohol-dependent men were normotensive and 15 (30%) hypertensive. Eighteen (51%) normotensive and 12 (80%) hypertensive subjects showed a significant decrease in 24 hr mean BP after ethanol withdrawal (mean decrease of 8.4 mm Hg [95% confidence interval, ,11.2 to ,5.7] and 12.5 mm Hg [confidence interval, ,16.2 to ,8.8], respectively) and were considered as sensitive to alcohol. The remaining alcohol-dependent subjects were considered as resistant to alcohol. Normotensive subjects sensitive to ethanol showed a significantly greater left ventricular mass and a significantly lower ejection fraction than those normotensive patients whose BP did not change after ethanol withdrawal (both p < 0.01). Conclusions: More than three fourths of the hypertensive and more than half of the normotensive alcohol-dependent patients showed sensitivity to the pressor effects of ethanol. Impairment also was observed in heart function in normotensive patients sensitive to the pressor effects of ethanol. [source] The haemodynamic response to propranolol in cirrhosis with arterial hypertension: a comparative analysis with normotensive cirrhotic patientsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2010P. Sharma Aliment Pharmacol Ther 2010; 32: 105,112 Summary Background, Cirrhosis with arterial hypertension is not uncommon. Haemodynamic alterations in these patients and the effects of beta-blocker on hepatic venous pressure gradient (HVPG) and systemic haemodynamics have not been evaluated. Aims, To compare the systemic haemodynamic alterations in hypertensive and normotensive cirrhotics, and to investigate the effects of propranolol on these parameters. Methods, A retrospective analysis of consecutive hypertensive cirrhotic patients (n = 33) who underwent haemodynamic assessment and paired HVPG measurement was done. Normotensive cirrhotics (n = 50) served as controls. Results, Hypertensive patients had a significantly higher heart rate, systemic (SVRI), and pulmonary vascular resistance. There was a significant reduction in mean arterial pressure (MAP) in the hypertensive cirrhotic group from 112 (107,130) mmHg to 95 (77,114) mmHg (P < 0.01), but no change in the normotensives. SVRI remained the same in the hypertensive cirrhotic group, but it increased in the normotensives. There was no correlation between MAP reduction and HVPG reduction. Conclusions, The frequency of HVPG response with propranolol treatment in hypertensive cirrhotics is similar to normotensive cirrhotics. Propranolol treatment reduces MAP significantly in hypertensive patients with cirrhosis. Treatment with a nonselective beta-blocker is a good strategy for hypertensive cirrhotic patients. [source] Arterial Rigidity And Cardiovascular Sympathetic Tone In Hypertensive Obese And Type 2 Diabetic PatientsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2000P Valensi An increase of arterial rigidity and sympathetic activity has been suggested to contribute to essential hypertension. We have shown that vagal control of heart rate (HR) variations during standardized tests is similarly impaired in normotensive obese and type 2 diabetic patients. The aim was to compare cardiovascular vagosympathetic balance and the link between pulse pressure, an index of arterial rigidity, and sympathetic activity in normotensive and hypertensive obese and type 2 diabetic patients. Groups 1 and 2 consisted of 70 normotensive and 32 hypertensive obese patients, groups 3 and 4 of 18 normotensive and 14 hypertensive diabetic patients respectively. HR and blood pressure (BP) variations were studied with a plethysmographic system and spectral analysis (Finapres). During a 5 min-period at a controlled breathing rate, in the 4 groups, the high frequency peak of HR variations (vagal control) was significantly lower than in controls (19 healthy subjects), and the mid/high frequency peak ratio of HR variations was significantly increased. During a standing test, the mid-frequency peak of systolic BP variations (sympathetic activity) did not differ significantly in obese or diabetic patients, either normotensive or hypertensive, and in controls. This peak correlated significantly with pulse pressure in groups 2 and 4 and in the control group but not in groups 1 and 3. In conclusion, 1) spectral analysis confirms that in obese and diabetic patients vagal control of HR variations is similarly reduced and suggests that sympathetic activity is relatively increased ; 2) in hypertensive patients sympathetic tone is not higher than in normotensive ones, but may contribute to arterial rigidity. [source] Plasma Asymmetric Dimethylarginine, Symmetric Dimethylarginine, l -Arginine, and Nitrite/Nitrate Concentrations in Cats with Chronic Kidney Disease and HypertensionJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008R.E. Jepson Background: Chronic kidney disease (CKD) and hypertension have been associated with decreased bioavailability of nitric oxide (NO) and endothelial dysfunction. Increased concentrations of the endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) are implicated. Hypothesis: Plasma ADMA concentration is increased in cats with CKD and systemic hypertension corresponding to a decrease in total plasma nitrate/nitrite (NOx) availability. Decrease in systolic blood pressure (SBP) and proteinuria during treatment of hypertension with amlodipine besylate may be associated with increased NOx availability. Animals: Sixty-nine client-owned normotensive and hypertensive cats with variable azotemia. Methods: Plasma ADMA, symmetric dimethylarginine (SDMA), and l -arginine were measured simultaneously by hydrophilic-interaction liquid chromatography-electrospray tandem mass spectrometry in cats from 6 groups: normotensive nonazotemic (n = 10), normotensive mildly azotemic (n = 10), hypertensive mildly azotemic with hypertensive retinopathy (n = 20), hypertensive mildly azotemic without hypertensive retinopathy (n = 10), normotensive moderately azotemic cats (n = 10), and hypertensive nonazotemic cats (n = 9). Plasma NOx concentrations were measured. Results: A moderate correlation between plasma creatinine and ADMA (n = 69, r= .608, P < .001), SDMA (n = 69, r= .741, P < .001), and NOx concentrations (n = 69, r= .589, P < .001) was observed. There was no association among plasma ADMA, SDMA, and NOx concentrations and SBP. Conclusions and Clinical Importance: Plasma ADMA and SDMA concentrations are increased in cats with CKD and correlate with plasma creatinine concentration. This may imply the presence of endothelial dysfunction in cats with CKD. Plasma ADMA concentrations were not associated with systemic hypertension. Treatment of systemic hypertension with amlodipine besylate did not affect plasma ADMA or NOx concentrations. [source] Remote Liver Injury is Attenuated by Adenovirus-Mediated Gene Transfer of Heme Oxygenase-1 During the Systemic Inflammatory Response SyndromeMICROCIRCULATION, Issue 7 2004SARAH D. MCCARTER ABSTRACT Objectives: Adenovirus-mediated gene therapy is being investigated with increasing success for future treatment of autoimmune diseases. However, the use of adenoviruses is still limited by inflammatory and immune responses in the target organ. Previous work by the authors' laboratory established that the adenovirus encoding inducible heme oxygenase (Ad-HO-1) does not elicit the acute hepatic inflammation normally caused by adenoviruses, inviting further investigation in models of severe inflammation. Concurrently, there is increasing evidence for an endogenous protective role for heme oxygenase (HO) in the liver during the systemic inflammatory response syndrome (SIRS). Building on our previous results, this study investigated the effect of Ad-HO-1 pretreatment on remote liver injury during normotensive SIRS, induced by bilateral hind limb ischemia and reperfusion. Methods: Microvascular perfusion and hepatocyte death were quantified using established intravital videomicroscopy techniques. Hepatocellular injury and liver function were assessed using blood-borne indicators. Results: Microvascular perfusion deficits and increased hepatocyte death occurred following limb ischemia and 3 h of reperfusion in vehicle-pretreated animals; however, Ad-HO-1 pretreatment prevented these deficits. In contrast, the increase in serum alanine transaminase levels was unaffected by Ad-HO-1 pretreatment. Serum bilirubin levels were increased during systemic inflammation, predominantly in the conjugated form; and, this increase was prevented by administration of Ad-HO-1. Conclusions: These data indicate that gene transfer of inducible HO is an effective method to protect the liver during SIRS, providing incentive for further investigation into gene therapy strategies exploiting this anti-inflammatory enzyme. [source] ORIGINAL ARTICLE: Human Serum Complement C3 and Factor H in the Syndrome of Hemolysis, Elevated Liver Enzymes, and Low Platelet CountAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2009Elif Ari Problem, Hemolysis, elevated liver enzymes, and low platelet count syndrome (HELLP syndrome) is a life-threatening variant of severe pre-eclampsia in pregnant women. The complement system may play a role in the pathogenesis of this condition. We sought to determine serum complement 3 (C3) levels and its regulatory protein complement factor H (FH) in the HELLP syndrome. Method of study, Twenty-two pre-eclamptic patients with HELLP syndrome (mean age: 27.8 ± 6.2 years), 21 pre-eclamptic patients without HELLP syndrome (mean age: 27.5 ± 6.8 years) and 24 normotensive, healthy pregnant women (mean age: 26.1 ± 4.4 years) were included in this study. Serum concentrations of C3 and FH were measured in all participants. Results, Concentrations of C3 and FH did not differ significantly between the study groups. In patients with the HELLP syndrome, FH levels were positively associated with platelet count. Conclusion, These findings did not support a major role of complement activation in the HELLP syndrome. In patients with HELLP, lower levels of FH are correlated with a reduced platelet count. [source] Erectile Function in Two-Kidney, One-Clip Hypertensive Rats is Maintained by a Potential Increase in Nitric Oxide ProductionTHE JOURNAL OF SEXUAL MEDICINE, Issue S3 2009A. Elizabeth Linder PhD ABSTRACT Introduction., Hypertension is closely associated with erectile dysfunction (ED) as it has been observed in many experimental models of hypertension. Additionally, epidemiological studies show that approximately a third of hypertensive patients have ED. Aim., To test the hypothesis that the two-kidney, one-clip (2K-1C) rat model of hypertension displays normal erectile function due to increased nitric oxide (NO) production in the penis. Methods., Ganglionic-induced increase in intracavernosal pressure (ICP)/mean arterial pressure (MAP) ratio was used as an index of erectile function in 2K-1C and in normotensive sham-operated (SHAM) anesthetized rats. Cavernosal strips from hypertensive and normotensive rats were used for isometric tension measurement. The contraction induced by alpha-adrenergic agonist phenylephrine and the relaxation induced by the NO donor sodium nitroprusside (SNP) and by the Rho-kinase inhibitor Y-27632 were performed in the absence and in the presence of the NO synthase inhibitor N, -nitro-L-arginine (L-NNA). Results., Changes in ICP/MAP induced by ganglionic stimulation were not different between 2K-1C and SHAM rats. The contractile response induced by phenylephrine as well as the relaxation induced by SNP or the Y-27632 were similar in cavernosal strips from both groups. However, in the presence of L-NNA, the relaxation induced by Y-27632 was significantly impaired in 2K-1C compared to SHAM. Conclusions., These data suggest that hypertension and ED could be dissociated from high levels of blood pressure in some animal models of hypertension. Erectile function in 2K-1C hypertensive rats is maintained in spite of the increased Rho-kinase activity by increased NO signaling. Linder AE, Dorrance AM, Mills TM, Webb RC, and Leite R. Erectile function in two-kidney, one-clip hypertensive rats is maintained by a potential increase in nitric oxide production. J Sex Med 2009;6(suppl 3):279,285. [source] Effects of lipopolysaccharide on vascular reactivity and mortality in ratsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 5-6 2002J. P. L. Nunes Summary 1 The effects of intraperitoneal (i.p.) lipopolysaccharide on vascular reactivity to noradrenaline in rat aorta under different conditions of passive tension, as well as on mortality in normotensive and hypertensive rats, were studied. 2 Concentration,response curves to noradrenaline were obtained in aorta rings, at two levels of passive tension: 3 and 0.5 g, from control and lipopolysaccharide-treated Wistar rats. Contractile responses were expressed as percentage of the maximal response to noradrenaline obtained in the beginning of the experiment at a resting tension of 2 g. The maxima were significantly larger (P < 0.05) at 3 g than at 0.5 g in both groups of rats: 117.8 vs. 62.3%, respectively, for control animals; 85.8 vs. 32.5%, respectively, for lipopolysaccharide-treated rats. 3 The 24-h mortality after the i.p. administration of lipopolysaccharide was lower in spontaneously hypertensive rats (1/12; 8%), when compared with control Wistar,Kyoto rats (5/11; 45%). However, mortality was higher in Wistar,Kyoto made hypertensive by 8-day administration of corticosterone (6/6; 100%). 4 We conclude that a differential sensitivity to noradrenaline of aortic smooth muscle at two different levels of passive tension is still present in lipopolysaccharide-treated animals. Chronic hypertension in SHR rats is associated with resistance to the lethal effects of lipopolysaccharide, whereas abrupt-onset hypertension induced by corticosterone leads to an increased mortality. 5 These results are compatible with the myofibrillary hypothesis, which explains vascular hyper-reactivity in chronic arterial hypertension, by postulating that a more favourable relative position (and/or proportion) for actin and myosin occurs, whereas in states of vascular hypo-reactivity, such as vasodilatory shock, the opposite phenomenon may exist. [source] Different sensitivity of isoprenaline-induced responses in ventricular muscle to sodium nitroprusside in normotensive and spontaneously hypertensive rats 1AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2000A. M. Manso 1 The aim of the present work was to study the possible modulatory role of nitric oxide (NO) on the positive inotropic effect induced by the ,-adrenoceptor agonist isoprenaline in myocardial contractility, and whether this modulation is altered by hypertension. 2 The study was performed using right ventricular strips from the hearts of 6-month-old male Wistar,Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The contractile force of electrically-stimulated ventricular strips was measured by a force-displacement transducer. 3 Isoprenaline (from 10 nmol l,1 to 10 ,mol l,1) induced a concentration-dependent increase in cardiac contractility in strips from both rat strains. This positive inotropic effect to isoprenaline was reduced by the NO donor sodium nitroprusside (SNP, 0.1 mmol l,1) in muscles from WKY rats and slightly increased in those from SHR. The SNP-induced increase in strips from SHR was abolished by superoxide dismutase (100 U ml,1). 4 NG-nitro-arginine-methyl ester (L-NAME, 0.1 mmol l,1) and 1H-[1,2,4]oxadiazolo[4,3]quinoxalin-1-one (ODQ, 10 ,mol l,1), respective inhibitors of NO synthase and guanylate cyclase, increased the response to isoprenaline in muscles from WKY rats, whereas it was unaltered in strips from SHR. 5 In strips from WKY rats, the combination of ODQ and SNP produced an increase in the response elicited by isoprenaline, which was similar to that observed with ODQ or L-NAME. 8-Br-cyclicGMP (8-Br-cGMP, 0.1 mmol l,1), a permeable and structural cGMP analogue, decreased the effect induced by isoprenaline only in muscles from WKY rats. 6 These results suggest that the positive inotropic response to isoprenaline in ventricular strips from WKY rats is negatively modulated by NO, and positively by superoxide anions in those from SHR. The lack of a modulatory response to NO in ventricular strips from SHR is probably a result of an alteration of mechanisms in NO-signalling pathway downstream of cGMP formation in SHR hearts. [source] Central Bromocriptine-Induced Tachycardia is Reversed to Bradycardia in Conscious, Deoxycorticosterone Acetate-Salt Hypertensive RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2001Saad Lahlou The present study investigated the effect of bromocriptine on heart rate and the principal site of action of this agonist in conscious, deoxycorticosterone acetate-salt hypertensive rats, in which altered central dopaminergic activity has been previously reported. Intravenous administration of bromocriptine (150 ,g/kg) increased heart rate (49±5 beats/min.) in uninephrectomized control rats, while it induced a significant bradycardia (50±6 beats/min.) in deoxycorticosterone acetate-salt hypertensive rats. In the latter animals, intravenous (500 ,g/kg) or intrathecal (40 ,g/rat at T9,T10) pretreatment with domperidone, a selective dopamine D2 receptor antagonist that does not cross the blood-brain barrier, reduced partially, but significantly, the bradycardiac responses to bromocriptine (reduction of about 44% and 48% of the maximal effect, respectively). In contrast, the bromocriptine-induced bradycardia was fully abolished by intravenous pretreatment with metoclopramide (300 ,g/kg), a dopamine D2 receptor antagonist that crosses the blood-brain barrier, or by combined pretreatment with intravenous and intrathecal domperidone. These results indicate that, in deoxycorticosterone acetate-salt hypertensive rats, bromocriptine decreases rather than increases heart rate, an effect that is mediated partly through a peripheral D2 dopaminergic mechanism and partly through stimulation of spinal dopamine D2 receptors. They further support the concept that, in normotensive, conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at both peripheral and spinal dopamine D2 receptors. [source] The interrelationship of complement-activation fragments and angiogenesis-related factors in early pregnancy and their association with pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 4 2010AM Lynch Please cite this paper as: Lynch A, Murphy J, Gibbs R, Levine R, Giclas P, Salmon J, Holers V. The interrelationship of complement-activation fragments and angiogenesis-related factors in early pregnancy and their association with pre-eclampsia. BJOG 2010; 117:456,462. Objective, To determine the interrelationships during early pregnancy of complement-activation fragments Bb, C3a and sC5b-9, and angiogenesis-related factors placental growth factor (PiGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), and their associations with pre-eclampsia. Design, Prospective cohort study. Setting, Denver complement study (June 2005,June 2008). Population, A total of 668 pregnant women with singleton gestations, recruited between 10 and 15 weeks of gestation. Methods, Using univariable and multivariable logistic regression analysis, concentrations of complement-activation fragments and angiogenesis-related factors were compared between 10 and 15 weeks of gestation in women who subsequently did or did not develop pre-eclampsia. Interrelationships between these variables were tested using the non-parametric Spearman rank correlation coefficient. Main outcome measure, Pre-eclampsia. The association of complement-activation fragments and angiogenesis-related factors with obesity was also examined. Results, The mean (±SD) levels of complement Bb in early pregnancy among women who did and did not develop pre-eclampsia were 0.84 (±0.26) ,g/ml and 0.69 (±0.2) ,g/ml, respectively (P = 0.001). Concentrations of PiGF were significantly (P = 0.01) lower (31 ± 12 pg/ml) in early pregnancy in the pre-eclamptic group of women, as compared with the normotensive group (39 ± 32 pg/ml). The adjusted odds ratio (AOR) of Bb and PiGF were 2.1 (CI = 1.4,3.1, P < 0.0003) and 0.2 (CI = 0.07,0.7, P = 0.01), respectively. There was no significant difference in the levels of C3a, sC5b-9, sFlt-1 and sEng in early pregnancy among women who developed pre-eclampsia, compared with women who remained normotensive during pregnancy. Higher levels of Bb (P = 0.0001) and C3a (P = 0.03), and lower levels of sFlt-1 (P = 0.0002) and sEng (P = 0.0001) were found among women with obesity, compared with non-obese controls. No meaningful relationships were found between the complement-activation fragments and the angiogenesis-related factors. Conclusions, In this cohort during early pregnancy, increased concentrations of complement-activation factor Bb and lower concentrations of PiGF were associated with the development of pre-eclampsia later in pregnancy. [source] Low plasma volume following pregnancy complicated by pre-eclampsia predisposes for hypertensive disease in a next pregnancyBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 11 2003Robert Aardenburg Objective A large number of women with a history of pre-eclampsia/HELLP have a low plasma volume at least six months postpartum. The objective of this study was to determine whether a low plasma volume in formerly pre-eclamptic women and HELLP patients is associated with an increased risk for recurrent hypertensive complications in a next pregnancy. Design Prospective observational study. Setting Tertiary obstetric centre. Sample Formerly pre-eclamptic women and controls. Methods In 316 women with a history of pre-eclampsia and/or HELLP, we measured, plasma volume along with haemodynamic, metabolic and haemostatic variables at least six months postpartum. A group of 22 healthy parous controls was used as a reference. After standardising plasma volume for body mass index, women were subdivided into normotensive and normal plasma volume (n = 199), normotensive and low plasma volume (n = 76) and hypertensive (n = 41) subgroups, which were compared for demography, clinical parameters and course of a next pregnancy. Main outcome measures Recurrent hypertensive disease of pregnancy. Results Relative to the normal plasma volume subgroup, normotensive women in the low plasma volume subgroup have a higher body mass index, a lower total vascular compliance and a shorter estimated systemic circulation time. They have a higher HOMA index and higher fasting triglyceride levels. In normotensive and hypertensive former patients alike, low plasma volume is associated with a higher recurrence of hypertensive complications in a next pregnancy compared with normotensive women with normal plasma volume. Conclusion Low plasma volume in normotensive women with a history of pre-eclampsia and/or HELLP is associated with overweight, reduced vascular compliance and insulin resistance and a predisposition for recurrent pre-eclampsia and HELLP syndrome in a next pregnancy. [source] Maternal serum activin, inhibin, human chorionic gonadotrophin and ,-fetoprotein as second trimester predictors of pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2003Emma J. Davidson Objective To compare the serum levels of human chorionic gonadotrophin (hCG), ,-fetoprotein, activin A, inhibin A and inhibin isoforms containing pro and ,C in the second trimester serum of women who subsequently developed hypertensive disorders of pregnancy with those who remained normotensive throughout pregnancy. Design Retrospective case,control study of 15,20 week serum samples matched for duration of storage at ,20°C. Setting Antenatal clinics at a teaching hospital in Scotland. Sample Second trimester serum samples of 39 women who subsequently developed pre-eclampsia, 31 who subsequently developed pregnancy-induced hypertension and 155 women who remained normotensive throughout pregnancy. Main outcome measures hCG, ,-fetoprotein, activin A, inhibin A and inhibin pro,,C serum levels. Results Activin A levels in serum were significantly elevated in women who later developed pregnancy-induced hypertension (26% increase compared with controls) and hCG levels were significantly elevated in women who later developed pre-eclampsia (24% increase compared with controls). ,-Fetoprotein, inhibin A and inhibin pro,,C levels were not significantly elevated in the patient groups compared with their controls. Conclusions A combination of analyses including second trimester serum activin A and hCG may yet prove to be helpful predictors of women at risk of hypertensive disorders of pregnancy. While the results proved significant, the effects reported in this study are too modest compared with natural variability to be useful as screening tools on their own. [source] Plasma P-selectin is elevated in the first trimester in women who subsequently develop pre-eclampsiaBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 7 2001P.M. Bosio Objective To report plasma concentrations of the adhesion cell molecule P-selectin during pregnancy to determine the effect of subsequent development of hypertension and pre-eclampsia. Design A longitudinal study. Methods A longitudinal study involving 70 women followed up from early pregnancy; 20 who subsequently developed pre-eclampsia were compared with 24 who developed gestational hypertension and 26 normotensive women with normal obstetric outcome. The determination of citrate plasma soluble P-selectin levels throughout pregnancy was performed using a commercial quantitative sandwich immunoassay kit. The temporal course of plasma P-selectin in the three groups of subjects was analysed. Results There was no significant difference in mean plasma P-selectin concentration between normotensive and gestational hypertensive subjects at any stage of pregnancy. Using a cutoff level of 60 ng/mL, P-selectin concentration at 10,14 weeks had a negative predictive value for pre-eclampsia of almost 99%. Mean plasma P-selectin concentrations were significantly elevated by 10,14 weeks in women who later developed pre-eclampsia (P<0.001). Conclusions Our data support an inflammatory model for pre-eclampsia whereby endothelial cell activation may be secondary to a primary inflammatory response. Plasma P-selectin has significant potential as a first trimester clinical marker of pre-eclampsia. [source] | |||||||||||||||||||||||||||||||||||||