JOURNAL OF FOOD BIOCHEMISTRY, Issue 3 2010
MARCIA DA SILVA PINTO
ABSTRACT Red currants (Ribes rubrum L.), black currants (Ribes nigrum L.), red and green gooseberries (Ribes uva-crispa) were evaluated for the total phenolics, antioxidant capacity based on 2, 2-diphenyl-1-picrylhydrazyl radical scavenging assay and functionality such as in vitro inhibition of ,-amylase, ,-glucosidase and angiotensin I-converting enzyme (ACE) relevant for potential management of hyperglycemia and hypertension. The total phenolics content ranged from 3.2 (green gooseberries) to 13.5 (black currants) mg/g fruit fresh weight. No correlation was found between total phenolics and antioxidant activity. The major phenolic compounds were quercetin derivatives (black currants and green gooseberries) and chlorogenic acid (red currants and red gooseberries). Red currants had the highest ,-glucosidase, ,-amylase and ACE inhibitory activities. Therefore red currants could be good dietary sources with potential antidiabetes and antihypertension functionality to compliment overall dietary management of early stages of type 2 diabetes. [source]

A FATAL HYPOTENSION BY SILDENAFIL IN AN END-STAGE RENAL DISEASE PATIENT WITH HYPERTENSION AND ABNORMAL PHARMACOKINETICS OF THE MEDICINE

NEPHROLOGY, Issue 3 2009
YOSHIHIRO WADA
[source]

ATYPICAL REVERSIBLE POSTERIOR LEUKOENCEPHALOPATHY SYNDROME IN A CHRONIC HAEMODIALYSIS PATIENT WITH SEVERE HYPERTENSION

NEPHROLOGY, Issue 6 2008
JONGHA PARK
[source]

IS SCLERODERMA RENAL CRISIS WITH ANTI-CENTROMERE ANTIBODY-POSITIVE LIMITED CUTANEOUS SYSTEMIC SCLEROSIS OVERLOOKED IN PATIENTS WITH HYPERTENSION AND/OR RENAL DYSFUNCTION?

NEPHROLOGY, Issue 2 2008
TOSHIRO SUGIMOTO
[source]

HYPERTENSION AS A DETERMINANT OF SURVIVAL FOR DIALYSIS PATIENTS

NEPHROLOGY, Issue 1 2002
Lynn Kl
[source]

CONTINUOUS FLUOXETINE ADMINISTRATION PREVENTS RECURRENCE OF PULMONARY ARTERIAL HYPERTENSION AND PROLONGS SURVIVAL IN RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2009
Shao-Ping Zhu
SUMMARY 1The serotonin transporter (SERT) is strongly implicated in the pathogenesis of pulmonary arterial hypertension (PAH) in patients and animal models. Inhibitors of SERT have been reported to attenuate or reverse experimental PAH, which makes them potential therapeutic options for the treatment of PAH in humans. However, little is known about pathophysiological features after reversal or attenuation of PAH; moreover, the long-term therapeutic effects of SERT inhibitors on PAH remain undetermined. Thus, the aim of the present study was to investigate the short- and long-term effects of fluoxetine on monocrotaline (MCT)-induced PAH and associated pathophysiological changes in PAH models. 2Rats were randomly divided into four groups as follows: (i) an M + F group, in which rats received a single injection of MCT (60 mg/kg, s.c.) and then after 3 weeks were given fluoxetine (10 mg/kg) once daily by gavage from Week 4 to Week 12; (ii) an M/F group, in which 3 weeks after a single MCT (60 mg/kg, s.c.) injection, rats were given fluoxetine (10 mg/kg) by daily gavage from Week 4 to Week 6 and were then given an equivalent volume of saline once daily by gavage from Week 7 to Week 12; (iii) an MCT group, in which 3 weeks after a single MCT (60 mg/kg, s.c.) injection rats were given an equivalent volume of saline by gavage from Week 4 to Week 12; and (iv) a saline group, in which rats received an equivalent volume of saline injection or gavage over the 12 week treatment period. Morphometric changes, pulmonary arterial pressure, percentage wall thickness, right ventricular hypertrophy index and SERT expression were detected at various times during the 12 week treatment period. Survival analysis was performed in each group. 3After 12 weeks treatment, it was found that even through fluoxetine treatment resulted in complete reversal of PAH, PAH recurred after fluoxetine withdrawal. In contrast, continuous administration of fluoxetine prevented the recurrence of PAH and prolonged survival. Analysis of SERT protein levels in rat lung indicated that, compared with values obtained at Week 0, SERT protein increased significantly after discontinuation of fluoxetine but continuous fluoxetine administration inhibited this increase. 4In conclusion, SERT overexpression correlates with the recurrence of PAH after withdrawal of fluoxetine in rats. Continuous fluoxetine administration prevents recurrence of PAH and prolongs survival. [source]

MELATONIN REDUCES BLOOD PRESSURE IN RATS WITH STRESS-INDUCED HYPERTENSION VIA GABAA RECEPTORS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2009
Hua-Li Li
SUMMARY 1Several groups have reported that melatonin produces a significant decrease in blood pressure in mammals and that pinealectomy in rats causes hypertension. The purpose of the present study was to investigate the effects of melatonin and bicuculline methiodide on the blood pressure of rats, both in the developing and fully developed stage of stress-induced hypertension (SIH). 2Rats with SIH were generated by mild electric foot shocks for 15 days, after which tail arterial systolic pressure and plasma angiotensin (Ang) II levels were measured. The effects of melatonin injections (i.p. or i.c.v.) on mean arterial pressure (MAP) in rats with SIH were also determined. 3Pretreatment with 1 mg/kg, i.p., melatonin significantly diminished the elevated tail arterial systolic pressure and plasma AngII levels caused by 15 days stress. The suppressive effects of melatonin were blocked by i.p. injection of 1 mg/kg bicuculline methiodide, an antagonist of the GABAA receptor. 4Intraperitoneal (0.2, 0.5 and 1 mg/kg) or i.c.v. (0.15 and 1.5 µg/3 µL) injection of melatonin produced a dose-dependent lowering of MAP in rats with SIH. The antihypertensive response induced by melatonin was blocked by injection of both 1 mg/kg, i.p., and 1.5 × 106 µg/3 µL, i.c.v., bicuculline methiodide. 5In conclusion, melatonin not only prevents increases in blood pressure during the developing stage of SIH, but can also reduce the blood pressure of rats that have already developed SIH. The antihypertensive effect of melatonin may be mediated by GABAA receptors through inhibition of plasma AngII levels. [source]

ANGIOTENSIN AT2 RECEPTOR AS A POTENTIAL THERAPEUTIC TARGET IN HYPERTENSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1 2009
Wing Tak Wong
No abstract is available for this article. [source]

EFFECTS OF MELATONIN ON BLOOD PRESSURE IN STRESS-INDUCED HYPERTENSION IN RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2008
Chun-Mei Xia
SUMMARY 1Melatonin, acting through its receptors, is involved in numerous physiological processes, including blood pressure (BP) regulation. In present study, the effect of melatonin inhibition on stress-induced hypertension was investigated. 2The hypertensive model consisted of male Sprague-Dawley rats subjected to electrical foot-shock combined with noise. Microinjection of melatonin (0.1 and 1.0 mmol/L) into the anterior hypothalamic area (AHA) produced a fall in BP in nomortensive rats and stress-induced hypertensive rats (SIHR). Luzindole (10 mmol/L), a competitive antagonist of melatonin MT1 and MT2 receptors, almost completely abolished the depressor effect of melatonin, the MT2 receptor-specific antagonist 4-phenyl-2-propionamidotetralin (10 mmol/L) partially blocked (by approximately 60%) the depressor effect of melatonin, whereas the MT3 receptor-selective antagonist prazosin (10 mmol/L) failed to antagonize the effects of melatonin. 3Brain microdialysis was performed in the AHA and the rostral ventrolateral medulla (RVLM). Melatonin and amino acids in the dialysate samples collected were detected by high-performance liquid chromatography combined with fluorescence detection. The results indicated that melatonin concentrations in the AHA were reduced in SIHR. Microinjection of melatonin into the AHA decreased glutamate release and increased GABA and taurine release in the RVLM, which were paralleled by a decrease in arterial pressure. 4The mRNA expression of MT2 in the AHA of SIHR was higher than that in normotensive control rats, whereas there was no significant difference in MT1 mRNA expressin between the two groups. 5The results of the present study suggest that both a decrease of melatonin and an increase in the MT2 receptor in the AHA are involved in the manifestation of stress-induced hypertension. Both MT1 and MT2 receptors participated in the antihypertensive effect of melatonin in the AHA. The antihypertensive effect of melatonin was related to the decreases in the excitatory amino acid glutamate and increases in the inhibitory amino acids taurine and GABA in the RVLM. [source]

STUDY OF THE RELATIONSHIP BETWEEN THE KAZAKH'S LIFESTYLE AND GENETIC FACTORS, AND HYPERTENSION, IN THE NORTH-WEST OF CHINA

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2007
NF Li
SUMMARY 1We investigated the relationship between genetic and environmental factors in hypertensive people living in the Xinjiang Uygur Autonomous Region of China. 2Body mass index, alcohol intake, serum total cholesterol, low-density lipoprotein-cholesterol and triglyceride level in the hypertensive group were significantly higher than corresponding values in the normal group. 3Angiotensinogen gene polymorphisms and related haplotype H6 and H9 were strongly associated with essential hypertension. The b2 -adrenergic receptor gene was associated with lipid disorders in Kazakhs in Xinjiang. 4The results suggest that both genetic and environmental factors play an important role in the development of hypertension in Kazakhs in Xinjiang. [source]

INTERPLAY OF REACTIVE OXYGEN SPECIES AND NITRIC OXIDE IN THE PATHOGENESIS OF EXPERIMENTAL LEAD-INDUCED HYPERTENSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2007
ND Vaziri
SUMMARY 1Lead is a common environmental and industrial toxin that can cause a variety of acute and chronic illnesses. For example, chronic exposure to low levels of lead has been shown to raise arterial pressure and promote renal and cardiovascular complications. 2Several mechanisms have been identified by which chronic lead exposure can cause hypertension and cardiovascular disease. In recent years, increasing evidence has emerged pointing to the role of oxidative stress as a major mediator of lead-induced hypertension. 3The present article provides an overview of the published studies on this subject. [source]

EFFECT OF BAY 41-2272 IN THE PULMONARY HYPERTENSION INDUCED BY HEPARIN,PROTAMINE COMPLEX IN ANAESTHETIZED DOGS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2007
Cristiane F Freitas
SUMMARY 1BAY 41-2272 is a potent activator of the nitric oxide-independent site of soluble guanylate cyclase and has been recently introduced as a new therapeutic agent to treat chronic pulmonary hypertension (PH) in neonatal sheep. Because the in vivo heparin,protamine interaction may lead to severe PH, the aim of the present study was to evaluate the effects of BAY 41-2272 in the PH induced by heparin,protamine interaction in anaesthetized dogs. 2Sixteen male dogs (10 mongrel dogs and six Beagles) were anaesthetized and instrumented for acquisition of mean arterial blood pressure (MABP), mean pulmonary arterial pressure (MPAP), heart rate (HR), pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and indices of systemic and pulmonary vascular resistance (ISVR and IPVR, respectively). Plasma cGMP levels and Spo2 were evaluated. 3Intravenous administration of heparin (500 IU/kg) followed 3 min later by protamine (10 mg/kg) caused marked PH, as evaluated by the increase in MPAP, PCWP and IPVR. This was accompanied by a significant fall in MABP and a transient increase in HR. Infusion of BAY 41-2272 (10 µg/kg per h, starting 10 min before heparin administration) augmented plasma cGMP levels and slightly and significantly increased HR and CI, without affecting the other cardiovascular parameters. The elevation in IPVR, MPAP and PCWP triggered by the heparin,protamine interaction was significantly reduced in animals exposed to BAY 41-2272. 4In vehicle-treated dogs, the Spo2 values decreased significantly at the peak of the PH and this was significantly attenuated by treatment with BAY 41-2272. In addition, BAY 41-2272 (10 µmol/L) had no effect on the activated partial thromboplastin time of citrated plasma after the addition of heparin,protamine. 5In conclusion, BAY 41-2272 was effective in reducing canine PH induced in vivo by the heparin,protamine interaction, thus indicating its potential in the treatment of this type of disorder. [source]

ROLE OF HYPOTHALAMIC ,2 -ADRENOCEPTOR ACTIVITY IN FRUCTOSE-INDUCED HYPERTENSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2006
Marcos A Mayer
SUMMARY 1The aim of the present study was to investigate the effects of the ,2 -adrenoceptor antagonist yohimbine on blood pressure and heart rate (HR) regulation, as well as on adrenergic and serotoninergic neurotransmission, in fructose hypertensive (F) rats. 2The anterior hypothalamic area of control (C) and F rats was perfused with Ringer's solution containing 10 and 100 µg/mL yohimbine through a microdialysis concentric probe. The effects of yohimbine on mean arterial pressure (MAP) and HR, as well as on hypothalamic dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5-HIAA) levels, were measured according to perfusion time. 3Although intrahypothalamic perfusion of yohimbine increased blood pressure in C rats (,MAP 9 ± 1 and 11 ± 2 mmHg for 10 and 100 µg/mL yohimbine, respectively; P < 0.05 vs Ringer's perfusion), the ,-adrenoceptor antagonist did not modify MAP in F. Intrahypothalamic yohimbine had no effect on HR at either concentration tested. Intrahypothalamic perfusion of 10 and 100 µg/mL yohimbine increased DOPAC levels in C rats (135 ± 6 and 130 ± 5% of basal levels, respectively; both n = 6; P < 0.05 vs Ringer's perfusion), but not in F animals (115 ± 6 and 102 ± 6% of basal levels, respectively; both n = 6). In both C and F rats, yohimbine administration induced an increase in 5-HIAA dialysate levels. 4The results of the present study support the notion that ,2 -adrenoceptor tone of the anterior hypothalamus of normotensive rats, which contributes to normal blood pressure regulation, is not involved in the control of HR in either normotensive C or hypertensive F rats. The absence of changes in MAP after yohimbine perfusion in F rats suggests that the ,2 -adrenoceptor tone could be decreased in this group of rats and that this may be responsible for the maintenance of hypertension in this model. Intrahypothalamic perfusion of yohimbine increased DOPAC in the dialysate only in C rats, suggesting changes in presynaptic ,2 -adrenoceptor activity in fructose-overloaded rats. Conversely, increased 5-HIAA levels did not differ between C and F groups. [source]

SPECIES VARIABILITY IN CARDIOVASCULAR RESEARCH: THE EXAMPLE OF ADRENOCORTICOTROPHIN-INDUCED HYPERTENSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2006
Judith A Whitworth
SUMMARY 1Lawrie Beilin has contributed greatly to international hypertension research through both animal and human studies. 2Animals are used in biomedical research to gain insights that can be extrapolated ultimately to humans. 3A simple experimental manipulation, adrenocorticotrophin (ACTH) administration, has a range of different cardiovascular effects in different species. 4Caution should be exercised in extrapolating data from animals to humans. [source]

HYPERTENSION, OBESITY AND GNB3 GENE VARIANTS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2006
María E Danoviz
SUMMARY 1The polymorphism C825T of the gene encoding the G-protein b3-subunit (GNB3) was found to be associated with an increased prevalence of hypertension in a number of studies. The aim of the present study was to investigate the association between this polymorphism and blood pressure phenotypes in an urban, large and ethnically mixed population of Brazil. 2Individuals (n = 1 568) were randomly selected from the general population of the Vitória City metropolitan area. The GNB3 C825T polymorphism was genotyped in each individual. Baseline cardiovascular risk factors were collected for all participants. Cardiovascular risk variables and genotypes were compared using anova and the Chi-squared test for univariate comparisons and logistic regression for multiple comparisons. 3A statistically significant interaction between the 825T allele and obesity was observed for systolic blood pressure (SBP; P = 0.02). In fact, the C825T genotype was predictive of SBP only in individuals with increased body mass index (P = 0.02). In addition, in a multiple logistic regression model conducted in the obese population and adjusted for age, sex, ethnicity, diabetes, triglycerides and total cholesterol, the presence of the T allele was significantly associated with a 1.5-fold (95% confidence interval 1.04,2.26) increased risk of hypertension. Lack of statistical power does not explain the absence of other positive gene,environment interactions. 4The present results suggest that an important gene ¥ environment interaction may take place between bodyweight regulation and the GNB3 gene. This finding provides further evidence for a role of the 825T allele in hypertension susceptibility and may be used for better disease stratification. [source]

RELATIVE CONTRIBUTION OF THE PRENATAL VERSUS POSTNATAL PERIOD ON DEVELOPMENT OF HYPERTENSION AND GROWTH RATE OF THE SPONTANEOUSLY HYPERTENSIVE RAT

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2006
Robert Di Nicolantonio
SUMMARY 1To determine the relative roles of the prenatal and postnatal (preweaning) environment on the development of blood pressure and growth rate in the spontaneously hypertensive rat (SHR) of the Okamoto strain, we used combined embryo transfer and cross-fostering techniques between SHR and normotensive Wistar-Kyoto (WKY) rats to produce offspring whose development was examined during the first 20 weeks of life. 2We measured litter sizes, bodyweights and tail-cuff blood pressures in offspring at 4, 8, 12 and 20 weeks of age. We also recorded heart, kidney and adrenal weights at 20 weeks of age, when the study concluded. 3We found that both the in utero and postnatal environments provided by the SHR mother could significantly affect WKY rat offspring growth rates, but blood pressure was unaffected in this strain. In SHR offspring, the SHR maternal in utero and suckling period both contributed to the rate of blood pressure development in the SHR, but not the final blood pressure of offspring at 20 weeks of age. This effect was greater for male than female offspring. Organ weights were largely unaffected by the perinatal environment in either strain. 4We conclude that although the SHR maternal in utero and immediate postnatal environment both contribute to the rate of blood pressure development in the SHR, they do not appear to contribute to the final blood pressure of offspring at maturity. The SHR maternal environment also alters growth rate that may, in turn, underlie these effects on SHR blood pressure development, particularly in males. [source]

GANGLION BLOCKADE DOES NOT PREVENT CORTISOL-INDUCED HYPERTENSION IN MAN

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2005
Paula M Williamson
SUMMARY 1.,The aim of the present study was to assess the effect of ganglion blockade on blood pressure in cortisol treated human subjects. 2.,Four healthy male subjects were treated with cortisol 80 mg/day for a 5-day period. Ganglion blockade was achieved by intravenous trimethaphan. 3.,Ganglion blockade did not significantly alter blood pressure in the pretreatment phase or on the last day of cortisol treatment. 4.,Taken together with our previous observations that sympathetic activity is unaltered or reduced by cortisol, these results suggest that cortisol induced hypertension in humans is not a result of overactivity of the autonomic nervous system. [source]

EFFECTS OF VITAMIN E AND SESAMIN ON HYPERTENSION AND CEREBRAL THROMBOGENESIS IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2004
Takanori Noguchi
SUMMARY The preventive effects of sesamin, a lignan from sesame oil and vitamin E on hypertension and thrombosis were examined using stroke-prone spontaneously hypertensive rats (SHRSP). Animals at 5 weeks of age were separated into four groups: (i) control group; (ii) vitamin E group, which was given 1000 mg alpha-tocopherol/kg diet; (iii) sesamin group, given 1000 mg sesamin/kg diet; and (iv) vitamin E plus sesamin group, given 1000 mg alpha-tocopherol plus 1000 mg sesamin/kg diet for 5 weeks from 5 to 10 weeks of age. Resting blood pressure was measured by the tail-cuff method once weekly. A closed cranial window was created in the right parietal bone of the rat and platelet-rich thrombi were induced in vivo using a helium-neon laser technique. The number of laser pulses required for formation of an occlusive thrombus was used as an index of thrombotic tendency. In control rats, systolic blood pressure and the amount of urinary 8-hydroxy-2,-deoxyguanosine (8-OHdG) became significantly elevated with age. However, the elevation in blood pressure and 8-OHdG were significantly suppressed in rats administered vitamin E, sesamin, or vitamin E plus sesamin. At 10 weeks, the number of laser pulses required to induce an occlusive thrombus in arterioles of the control group was significantly lower than in the other groups (P < 0.05). These results indicate that chronic ingestion of vitamin E and sesamin attenuated both elevation in blood pressure, oxidative stress and thrombotic tendency, suggesting that these treatments might be beneficial in the prevention of hypertension and stroke. [source]

Pulmonary Hypertension in Patients after Repair of Transposition of the Great Arteries

CONGENITAL HEART DISEASE, Issue 2 2010
Ellen Chan MD
ABSTRACT One well-documented complication of unrepaired d-transposition of the great arteries (d-TGA) is progressive pulmonary vascular disease. It is generally accepted that pulmonary vascular disease will not develop if d-TGA repair is performed early in life. Herein, we report a number of repaired d-TGA, especially in older patients with Mustard/Senning procedures, in whom pulmonary vascular disease developed years after their original repair. The etiology of this phenomenon is unknown, warranting further investigation. Our case reports highlight an overlooked, possible long-term complication following d-TGA repair. From this experience, we recommend that evidence of progressive pulmonary vascular disease may need to be regularly sought during the follow-up of patients after d-TGA repair, especially Mustard/Senning repairs, as early treatment of pulmonary hypertension may improve long-term clinical outcomes. [source]

Successful Treatment of an Adult Patient with an Aortopulmonary Window and Severe Unilateral Pulmonary Hypertension

CONGENITAL HEART DISEASE, Issue 6 2009
Olaf Franzen MD
ABSTRACT A 40-year-old woman with an aortopulmonary window combined with a severe stenosis of the right pulmonary artery was successfully treated by surgical closure of the defect and pulmonary artery patch plasty of the pulmonary stenosis. Even though the vasculature of the left lung was severely damaged preoperatively, the resulting pressure in the lung after surgical correction was only mildly elevated. [source]

Identifying Left Ventricular Dysfunction in Pulmonary Hypertension

CONGESTIVE HEART FAILURE, Issue 5 2009
Navin Rajagopalan MD
The significance of left ventricular (LV) dysfunction in patients with pulmonary hypertension (PH) is unknown. Our purpose was to quantify LV function in PH patients by measuring LV myocardial performance index (MPI) and correlating it with invasively determined hemodynamic variables. The authors prospectively measured LV MPI via transthoracic echocardiography in 50 patients with PH (53±11 years; 35 women) who also underwent right heart catheterization within 1 day of echocardiography. For comparative purposes, LV MPI was also measured in 15 healthy volunteers who served as controls. LV MPI was significantly increased in the PH group compared with controls (0.62±0.27 vs 0.36±0.08; P<.001), indicating worse LV dysfunction despite that LV ejection fraction was not significantly different between the groups (58%±4% vs 60%±3%). LV MPI demonstrated significant correlations with invasively determined mean pulmonary artery pressure (r=.50; P<.001), pulmonary vascular resistance (r=.57; P<.001), and cardiac index (r=,.64; P<.001). By receiver operating characteristic analysis, LV MPI >0.75 predicted cardiac index <2 L/min/m2 with 89% sensitivity and 78% specificity (area under the curve, 0.89). In a multivariate model, LV MPI was independently associated with cardiac index (P<.01). Patients with PH demonstrate abnormal LV function as quantified by elevated LV MPI, which correlates significantly with pulmonary vascular resistance and cardiac index. [source]

Successful Transition From Intravenous to Inhaled Prostacyclin in a Patient With Pulmonary Hypertension and Right Ventricular Failure

CONGESTIVE HEART FAILURE, Issue 5 2008
Madhavi T. Reddy MD
No abstract is available for this article. [source]

Correlation of Tricuspid Annular Velocities With Invasive Hemodynamics in Pulmonary Hypertension

CONGESTIVE HEART FAILURE, Issue 4 2007
Navin Rajagopalan
The authors performed tissue Doppler imaging of the tricuspid annulus in patients with pulmonary hypertension to assess its correlation with invasive indices of right ventricular function. The study population consisted of 32 patients with suspected pulmonary hypertension who underwent pulsed tissue Doppler imaging of the tricuspid annulus and right heart catheterization. Peak systolic (Sa), early diastolic (Ea), and late diastolic (Aa) velocities of the lateral tricuspid annulus were measured and correlated with hemodynamic variables. Peak Sa demonstrated excellent correlation with hemodynamic variables, including cardiac index (r=0.78; P<.001), pulmonary vascular resistance (r=,0.79; P<.001), and transpulmonary gradient (r=,0.72; P<.001). Peak Sa <10 cm/s predicted cardiac index <2.0 L/min/m2 with 89% sensitivity and 87% specificity. In conclusion, tissue Doppler imaging of the tricuspid annulus is a complementary method to assess right ventricular function in pulmonary hypertensive patients. [source]

Usefulness of B-Type Natriuretic Peptide as a Predictor of Treatment Outcome in Pulmonary Arterial Hypertension

CONGESTIVE HEART FAILURE, Issue 5 2004
Myung H. Park MD
We examined the utility of early modulation B-type natriuretic peptide (BNP) levels in 20 pulmonary arterial hypertension patients as a marker of response to epoprostenol therapy. The baseline BNP level was 828±217 pg/mL. A total of 19 hospitalizations and one death occurred in nine patients during 11.0±1.8 months. At baseline, a trend toward higher BNP level was observed among the event-free (Group A) as compared with clinical event patients (Group B) (1090±372 vs. 510±235 pg/mL, respectively; p=0.08). After 3 months on epoprostenol, a significant reduction among Group A occurred while Group B demonstrated an increase (288±92 vs. 610±121 pg/mL, p=0.04). A comparison of percent reduction in BNP level demonstrated a ,70±7% change among Group A and an 11±19% increase in Group B (p=0.005). A decrease in BNP level of ,50% during the first 3 months on epoprostenol was strongly predictive of event-free survival (p=0.003). This investigation establishes the utility of BNP for predicting response to epoprostenol therapy in pulmonary arterial hypertension. [source]

Comparison of Impedance Cardiography to Direct Fick and Thermodilution Cardiac Output Determination in Pulmonary Arterial Hypertension

CONGESTIVE HEART FAILURE, Issue 2004
Gordon L. Yung MD
Cardiac output (CO) is an important diagnostic and prognostic tool for patients with ventricular dysfunction. Pulmonary hypertension patients undergo invasive right heart catheterization to determine pulmonary vascular and cardiac hemodynamics. Thermodilution (TD) and direct Fick method are the most common methods of CO determination but are costly and may be associated with complications. The latest generation of impedance cardiography (ICG) provides noninvasive estimation of CO and is now validated. The purpose of this study was to compare ICG measurement of CO to TD and direct Fick in pulmonary hypertension patients. Thirty-nine enrolled patients were analyzed: 44% were male and average age was 50.8±17.4 years. Results for bias and precision of cardiac index were as follows: ICG vs. Fick (,0.13 L/min/m2 and 0.46 L/min/m2), TD vs. Fick (0.10 L/min/m2 and 0.41 L/min/m2), ICG vs. TD (respectively, with a 95% level of agreement between ,0.72 and 0.92 L/min/m2; CO correlation of ICG vs. Fick, TD vs. Fick, and ICG vs. TD was 0.84, 0.89, and 0.80, respectively). ICG provides an accurate, useful, and cost-effective method for determining CO in pulmonary hypertension patients, and is a potential tool for following responses to therapeutic interventions. [source]

Transgenic mice for studies of the renin,angiotensin system in hypertension

ACTA PHYSIOLOGICA, Issue 4 2004
J. L. Lavoie
Abstract Hypertension is a polygenic and multi-factorial disorder that is extremely prevalent in western societies, and thus has received a great deal of attention by the research community. The renin,angiotensin system has a strong impact on the control of blood pressure both in the short- and long-term, making it one of the most extensively studied physiological systems. Nevertheless, despite decades of research, the specific mechanisms implicated in its action on blood pressure and electrolyte balance, as well as its integration with other cardiovascular pathways remains incomplete. The production of transgenic models either over-expressing or knocking-out specific components of the renin,angiotensin system has given us a better understanding of its role in the pathogenesis of hypertension. Moreover, our attention has recently been refocused on local tissue renin,angiotensin systems and their physiological effect on blood pressure and end-organ damage. Herein, we will review studies using genetic manipulation of animals to determine the role of the endocrine and tissue renin,angiotensin system in hypertension. We will also discuss some untraditional approaches to target the renin,angiotensin system in the kidney. [source]

The role of renin,angiotensin,aldosterone system-based therapy in diabetes prevention and cardiovascular and renal protection

DIABETES OBESITY & METABOLISM, Issue 12 2008
Hussam Abuissa
Hypertension increases the risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease. In addition to lowering blood pressure, blockade of the renin,angiotensin,aldosterone system (RAAS) reduces the risk of new-onset T2DM and offers renal protection. Using a MEDLINE search, we identified multiple trials that reported the incidence of T2DM in patients taking inhibitors of RAAS. In this review, we will discuss the RAAS as a potential target in diabetes prevention and the mechanisms through which inhibitors of this system achieve such an important effect. We will also shed light on the beneficial cardiovascular and renal effects of RAAS blockade. Although multiple studies have demonstrated that inhibitors of RAAS, especially angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, can reduce the incidence of T2DM, randomized controlled studies are still needed to further elucidate their exact role in diabetes prevention. [source]