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Acute Increase (acute + increase)

Distribution by Scientific Domains

Medical Sciences	77%
Life Sciences	16%

Distribution within Medical Sciences

Pharmacology & Pharmaceutical Medicine	20%
Cardiovascular Disease	14%

Selected Abstracts

Acute increase in femoral artery resistance in response to direct physical stimuli in the human fetus

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 10 2003
Richard P. Smith
Objective To determine whether fetal response to needling resembles the fetal ,brain sparing' response seen with hypoxaemia. Design Prospective observational study. Setting Centre for Fetal Care, Queen Charlotte's and Chelsea Hospital, London. Population Eighty-five pregnant women undergoing invasive procedures associated with fetal prenatal diagnosis and/or management. Methods The femoral artery and the middle cerebral artery pulsatility index were measured by Doppler ultrasonography before and after 89 invasive procedures (fetal blood sampling, transfusion, bladder or cyst aspiration, shunt insertion and amniocentesis, between 17 and 36 weeks). Cases in which the fetal body was transgressed were compared with ,control' fetuses undergoing invasive procedures which did not directly involve needling the fetus (amniocentesis and placental cord insertion procedures). Main outcome measures Femoral artery and middle cerebral artery pulsatility index. Results The femoral artery pulsatility index rose after transgression [median change (,) 0.73; 95% confidence interval (CI) 0.51 to 0.98]. In contrast, there was no significant change in femoral artery pulsatility index after non-transgression procedures (mean , 0.28; 95% CI ,0.20 to 0.76). Analysis confirmed the fall in middle cerebral artery pulsatility index after transgression procedures (median ,,0.19; 95% CI ,0.07 to ,0.35), but there was also a significant fall in middle cerebral artery pulsatility index after non-transgression procedures (mean ,,0.47; 95% CI ,0.23 to ,0.71). Conclusions The human fetus mounts a peripheral haemodynamic response to invasive procedures involving transgression of the fetal body, which is consistent with the brain sparing effect. However, the change in middle cerebral artery pulsatility index in both transgression and control procedures suggests that the changes and mechanisms may be more complex than previously thought. [source]

Regulation of Blood,Brain Barrier Permeability

MICROCIRCULATION, Issue 2 2001
WILLIAM G. MAYHAN
ABSTRACT The blood-brain barrier minimizes the entry of molecules into brain tissue. This restriction arises by the presence of tight junctions (zonulae occludens) between adjacent endothelial cells and a relative paucity of pinocytotic vesicles within endothelium of cerebral arterioles, capillaries, and venules. Many types of stimuli can alter the permeability characteristics of the blood-brain barrier. Acute increases in arterial blood pressure beyond the autoregulatory capacity of cerebral blood vessels, application of hyperosmolar solutions, application of various inflammatory mediators known to be elevated during brain injury, and/or activation of blood-borne elements such as leukocytes can produce changes in permeability of the blood-brain barrier. The second messenger systems that account for increases in permeability of the blood-brain barrier during pathophysiologic conditions, however, remain poorly defined. This review will summarize studies that have examined factors that influence disruption of the blood-brain barrier, and will discuss the contribution of various cellular second messenger pathways in disruption of the blood-brain barrier during pathophysiologic conditions. [source]

Changes in mean arterial pressure predict degranulation of renomedullary interstitial cells

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2002
Christine Maric
Summary 1.,Renomedullary interstitial cells (RMIC) are characterized by numerous intracellular granules thought to contain renal medullary antihypertensive substances. However, the nature of the trigger for RMIC degranulation remains to be elucidated. The present study examines the effects of acute alterations in mean arterial pressure (MAP) and medullary blood flow (MBF) on RMIC granulation. 2.,Basal MAP and MBF in anaesthetized Sprague-Dawley rats (n = 4/group) were altered by intravenous infusions of vasoactive agents, including angiotensin II alone or with a nitric oxide (NO) synthase inhibitor (N, -nitro- l -arginine) or NO donor (sodium nitroprusside), noradrenaline and by carotid artery clamping. Following these treatments, kidneys were examined by electron microscopy and the absolute volume of granules in the renal medulla was calculated using unbiased stereological methods. 3.,Acute increases in MAP, regardless of the treatment causing the increase, were associated with a reduction in the absolute volume of granules in the range of 42,67%. Regression analysis revealed that only increases in MAP, but not MBF, strongly predict RMIC degranulation. 4.,Despite previous reports that changes in MBF activate renomedullary antihypertensive activity, we conclude that the change in MAP is an important determinant of the activity of the blood pressure-lowering mechanism of the renal medulla, with the assumption that the medullary lipids mediate the antihypertensive property of the renal medulla. [source]

Nerve growth factor increases airway responses and decreases levels of exhaled nitric oxide during histamine challenge in an in vivo guinea-pig model

ACTA PHYSIOLOGICA, Issue 2 2001
S. G. Friberg
There is a growing body of evidence supporting the idea that nerve growth factor (NGF) may be involved in the development of asthma-associated symptoms, such as airway hyper-responsiveness. Increased levels of NGF have recently been described in serum and in the airways of asthmatics. We have examined whether exhaled nitric oxide (NO) levels might be altered during the increased airway responses upon NGF treatment in guinea-pigs in vivo. Intravenous (i.v.) administration of histamine normally elicits a rapid peak in insufflation pressure (IP) and in exhaled NO, followed by a period of decreased concentrations of exhaled NO. Anaesthetized guinea-pigs were pre-treated intravenously with either saline, 4 or 80 ng kg,1 NGF 30 min before i.v. challenge with 16 ,g kg,1 histamine. At 80 ng kg,1 NGF significantly enhanced the airway obstruction caused by histamine, whereas the peak acute increase in exhaled NO was not enhanced. Following the increase, came a rapid drop, an effect enforced in the NGF treated animals. Subsequently, the time to return to 90% of resting exhaled NO was increased, from 12 min in saline-treated animals to 48 min in NGF-treated animals. Our data confirm that NGF can enhance airway responses to histamine. Moreover, our study shows a decrease in exhaled NO following a histamine challenge, an effect enhanced by NGF. A reduced ability to release exhaled NO may be a mechanism for increased airway responses during elevated NGF levels. The interaction between NGF and airway NO formation, and its relation to airway responses, merit further investigation. [source]

Behavioral economic analysis of cue-elicited craving for alcohol

ADDICTION, Issue 9 2010
James MacKillop
ABSTRACT Aims Craving as a motivational determinant of drug use remains controversial because of ambiguous empirical findings. A behavioral economic approach may clarify the nature of craving, theorizing that subjective craving functionally reflects an acute increase in a drug's value. The current study tested this hypothesis via a multidimensional assessment of alcohol demand over the course of an alcohol cue reactivity procedure. Design One-way within-subjects design. Setting Human laboratory environment. Participants Heavy drinkers (n = 92) underwent exposures to neutral (water) cues followed by personalized alcohol cues. Assessments Participants were assessed for craving, alcohol demand, affect, and salivation following each exposure. Findings Alcohol versus neutral cues significantly increased craving and multiple behavioral economic measures of the relative value of alcohol, including alcohol consumption under conditions of zero cost (intensity), maximum expenditure on alcohol (Omax), persistence in drinking to higher prices (breakpoint) and proportionate price insensitivity (normalized Pmax). Craving was significantly correlated with demand measures at levels ranging from 0.21,0.43. Conclusions These findings support the potential utility of a behavioral economic approach to understanding the role of environmental stimuli in alcohol-related decision making. Specifically, they suggest that the behavioral economic indices of demand may provide complementary motivational information that is related to though not entirely redundant with measures of subjective craving. [source]

Treatment of refractory fludarabine induced autoimmune haemolytic with the anti-cd20 monoclonal antibody rituximab

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2006
R. SWORDS
Summary A patient with cold-type autoimmune haemolytic anaemia for 8 years developed progressive B cell chronic lymphocytic leukaemia (CLL). Despite the risk of fludarabine induced exacerbation of haemolysis, he was given aggressive anti-CLL therapy with six courses of FCR (fludarabine 25 mg/m2 D1,3, cyclophosphamide 250 mg/m2 D2,4 and rituximab 375 mg/m2 D1) every 4 weeks. This resulted in a marked acute increase in haemolysis shortly after completing each course of fludarabine. However, haemolysis had settled to its baseline level by the time of subsequent courses of FCR. FCR resulted in complete clinical remission of CLL but residual haemolysis persisted. The patient was then given four weekly infusions of single agent rituximab, resulting in ongoing remission of haemolysis. In this patient, rituximab appears to have controlled fludarabine induced exacerbation of autoimmune haemolysis. In addition, subsequent single agent rituximab therapy resulted in prolonged remission of cold-type autioimmune haemolytic anaemia. It remains to be seen if the addition of rituximab will allow other patients with a positive direct Coomb's test and/or autoimmune haemolysis to receive fludarabine containing chemotherapy without undue risk of life-threatening haemolytic anaemia. [source]

Role of Inducible Nitric Oxide Synthase in Skeletal Adaptation to Acute Increases in Mechanical Loading,,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 6 2002
Makoto Watanuki M.D.
Abstract To clarify the role of nitric oxide (NO) in regulation of bone metabolism in response to skeletal loading, we examined inducible NO synthase (iNOS) gene knockout mice in the tail-suspension model. Histomorphometric analyses of proximal tibias revealed that 7 days of tail suspension decreased the bone volume (BV/TV) and bone formation rate (BFR/BS) and increased the osteoclast surface (Oc.S/BS) in mice with all iNOS genotypes. Both iNOS+/+ and iNOS+/, mice responded to subsequent 14-day reloading, with increases in BV/TV and BFR/BS and a decrease in Oc.S/BS, whereas these responses were abolished in iNOS,/, mice. The osteoblasts flattened after tail suspension appeared cuboidal during subsequent reloading. Immunoreactivity for iNOS was detected in these osteoblasts and osteocytes by immunohistochemistry. These defective responses after reloading were rescued in iNOS,/, mice by treatment with an NO donor nitroglycerine (NG). Conversely, the responses in iNOS+/+ mice were inhibited by treatment with an NOS inhibitor aminoguanidine (AG). In bone marrow cell cultures, mineralized nodules derived from iNOS,/, mice after reloading were significantly reduced. Taken together, our results suggest that NO generated by iNOS in osteoblasts plays a critical role in adjusting bone turnover and increasing osteogenic activity in response to the acute increase in mechanical loading after tail suspension. [source]

Temperature-dependent changes in energy metabolism, intracellular pH and blood oxygen tension in the Atlantic cod

JOURNAL OF FISH BIOLOGY, Issue 6 2003
F. J. Sartoris
The effect of acute increase in temperature on oxygen partial pressure (Po2) was measured in the gill arches of Atlantic cod Gadus morhua between 10 and 19° C by use of oxygen microoptodes. Oxygen saturation of the gill blood under control conditions varied between 90 and 15% reflecting a variable percentage of arterial or venous blood in accordance with the position of each optode in the gill arch. The data obtained suggested that arterial Po2 remained more or less constant and arterial oxygen uptake did not become limiting during warming. A progressive drop in venous Po2, however, was observed at >10° C indicating that excessive oxygen uptake from the blood is not fully compensated for by circulatory performance, until finally, Po2 levels fully collapse. In a second set of experiments energy and acid,base status of white muscle of Atlantic cod in vivo was measured by magnetic resonance (31P-NMR) spectroscopy in unanaesthetized and unimmobilized fish in the temperature range between 13 and 21° C. A decrease in white muscle intracellular pH (pHi) with temperature occurred between 10 and 16° C (,pH per ° C = ,0·025 per ° C). In white muscle temperature changes had no influence on high-energy phosphates such as phosphocreatine (PCr) or ATP except during exposure to high critical temperatures (>16° C), indicating that white muscle energy status appears to be relatively insensitive to thermal stress if compared to the thermal sensitivity of the whole animal. The data were consistent with the hypothesis of an oxygen limitation of thermal tolerance in animals, which is set by limited capacity of oxygen supply mechanisms. In the case of Atlantic cod circulatory rather than ventilatory performance may be the first process to cause oxygen deficiency during heat stress. [source]

Delirious episodes induced by intravenous administration of clomipramine associated with an acute increase in its plasma concentrations

PSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 6 2000
Nobuhisa Ueda MD
Abstract The aim of this paper is to describe two cases of clomipramine-induced delirium. One 61-year-old and one 67-year-old female depressive patients became delirious after beginning intravenous clomipramine injections in addition to their oral clomipramine administrations. Their plasma levels of both clomipramine and its metabolite, desmethylclomipramine, were acutely increased about twofold during delirium. The intravenous clomipramine administrations were discontinued. Their delirious state was gradually improved after stopping the intravenous clomipramine administrations. These findings suggest that acute increases of plasma levels of clomipramine and desmethylclomipramine after intravenous clomipramine injections might be related to the appearance of the delirious episodes. [source]

Prostaglandin F2, Stimulates Endothelial Nitric Oxide Synthase Depending on the Existence of Bovine Granulosa Cells: Analysis by Co-culture System of Endothelial Cells, Smooth Muscle Cells and Granulosa Cells

REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2008
K Shirasuna
Contents Prostaglandin F2, (PGF2,) induces luteolysis in the mid but not in the early luteal phase; despite this, both the early and the mid corpus luteum (CL) have PGF2, receptor (FPr). We previously indicated that the luteal blood flow surrounding the CL drastically increases prior to a decrease of progesterone (P) in the cows, suggesting that an acute increase of luteal blood flow may be an early sign of luteolysis in response to PGF2, and that this may be induced by a vasorelaxant nitric oxide (NO). The aim of this study was to investigate the luteal stage-dependent and the site-restricted effect of PGF2, and NO on the mRNA expressions and P secretion. To mimic the local luteal region both of peripheral and central areas of the CL, we utilized co-cultures using bovine aorta endothelial cells (EC), smooth muscle cells (SMC) and luteinizing granulosa cells (GC) or fully-luteinized GC. PGF2, stimulated the expression of endothelial NO synthase (eNOS) mRNA at 0.5 h in mix-cultures of EC and SMC with fully-luteinized GC but not with luteinizing GC. The expression of eNOS mRNA in EC was increased by PGF2, at 1 h only when EC was cultured together with fully-luteinized GC but not with luteinizing GC. In all co-cultures, PGF2, did not affect the mRNA expression of FPr. Treatment of NO donor inhibited P secretion at 0.5 h. In conclusion, the present study suggests that the coexistence of the mature luteal cells (fully-luteinized GC) with EC/SMC may be crucial for acquiring functional NO synthesis induced by PGF2,. [source]

Na+ -H+ exchanger 3 (NHE3) is present in lipid rafts in the rabbit ileal brush border: a role for rafts in trafficking and rapid stimulation of NHE3

THE JOURNAL OF PHYSIOLOGY, Issue 2 2001
Xuhang Li
1Rabbit ileal Na+ -absorbing cell Na+ -H+ exchanger 3 (NHE3) was shown to exist in three pools in the brush border (BB), including a population in lipid rafts. Approximately 50 % of BB NHE3 was associated with Triton X-100-soluble fractions and the other ,50 % with Triton X-100-insoluble fractions; ,33 % of the detergent-insoluble NHE3 was present in cholesterol-enriched lipid microdomains (rafts). 2The raft pool of NHE3 was involved in the stimulation of BB NHE3 activity with epidermal growth factor (EGF). Both EGF and clonidine treatments were associated with a rapid increase in the total amount of BB NHE3. This EGF- and clonidine-induced increase of BB NHE3 was associated with an increase in the raft pool of NHE3 and to a smaller extent with an increase in the total detergent-insoluble fraction, but there was no change in the detergent-soluble pool. In agreement with the rapid increase in the amount of NHE3 in the BB, EGF also caused a rapid stimulation of BB Na+ -H+ exchange activity. 3Disrupting rafts by removal of cholesterol with methyl-,-cyclodextrin (M,CD) or destabilizing the actin cytoskeleton with cytochalasin D decreased the amount of NHE3 in early endosomes isolated by OptiPrep gradient fractionation. Specifically, NHE3 was shown to associate with endosomal vesicles immunoisolated by anti-EEA1 (early endosomal autoantigen 1) antibody-coated magnetic beads and the endosome-associated NHE3 was decreased by cytochalasin D and M,CD treatment. 4We conclude that: (i) a pool of ileal BB NHE3 exists in lipid rafts; (ii) EGF and clonidine increase the amount of BB NHE3; (iii) lipid rafts and to a lesser extent, the cytoskeleton, but not the detergent-soluble NHE3 pool, are involved in the EGF- and clonidine-induced acute increase in amount of BB NHE3; (iv) lipid rafts and the actin cytoskeleton play important roles in the basal endocytosis of BB NHE3. [source]

Metformin Induces Cardioprotection against Ischaemia/Reperfusion Injury in the Rat Heart 24 Hours after Administration

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2008
Lasse Solskov
The energy sensing enzyme AMP-activated protein kinase (AMPK) has been indicated to play an important protective role in the ischaemic heart and is activated by metformin. The aim of this study was to determine whether a single dose of metformin protects the myocardium against experimentally induced ischaemia 24 hr after the administration, and furthermore to determine whether a single dose of metformin results in an acute increase in myocardial AMPK activity. Wistar rats were given either a single oral dose of metformin (250 mg/kg body weight), or a single oral dose of saline. After 24 hr, the hearts were Langendorff-perfused and subjected to 45 min. of coronary artery occlusion. Infarct size was determined by staining with triphenyltetrazoliumchloride (TTC) and Evans Blue and expressed as a percentage of the risk zone (IS/AAR %). Isoform specific AMPK activity was measured 2 hr after administration of metformin or saline. Infarct size was significantly reduced in the metformin treated (I/R: 19.9 ± 3.9%versus 36.7 ± 3.6%, P < 0.01, n = 8,14) compared to the control group. A single oral dose of metformin resulted in an approximately ~2-fold increase in AMPK-,2 activity 2 hr after administration (P < 0.015, n = 10). In conclusion, a single dose of metformin results in an acute increase in myocardial AMPK activity measured 2 hr after administration and induces a significant reduction in myocardial infarct size 24 hr after metformin administration. Increased AMPK activity may be an important signal mediator involved in the mechanisms behind the cardioprotective effects afforded by metformin. [source]

Response of retinal arteriole diameter to increased blood pressure during acute hyperglycaemia

ACTA OPHTHALMOLOGICA, Issue 3 2007
Peter Jeppesen
Abstract. Purpose:, To study retinal response in terms of arteriole diameter and retinal thickness secondary to an increase in arterial blood pressure during acute hyperglycaemia. Methods:, In a randomized, double-blinded, cross-over study, nine healthy persons were subjected to clamping of blood glucose to either 5 mmol/l or 15 mmol/l using somatostatin to control endogenous insulin secretion. The response of retinal arterioles in terms of diameter as determined with the retinal vessel analyser (RVA) and retinal thickness as assessed by optical coherence tomography (OCT) were measured after an increase in arterial blood pressure induced by isometric exercise. Arterial feeding pressure in the eye was assessed from the ophthalmic artery pressure and pulse amplitude measured by ophthalmodynamometry. Results:, Isometric exercise induced a significant increase in mean arterial blood pressure and a significant contraction of the retinal arterioles. An acute increase in blood glucose from 5 mmol/l to 15 mmol/l did not affect either the diameter of retinal vessels or retinal thickness. Conclusions:, Acute hyperglycaemia per se does not change isometric exercise-induced retinal arteriolar contraction. Metabolic factors other than blood glucose are suspected to be involved in the impairment of retinal autoregulation as seen in hyperglycaemia induced by oral glucose intake. [source]

Acute left ventricular failure after large volume pericardiocentesis

CLINICAL CARDIOLOGY, Issue 12 2003
A. Chamoun M.D.
Abstract This paper reports on two cases of large volume pericardiocentesis followed by transient severe acute left ventricular (LV) systolic failure in the absence of any prior history of LV dysfunction. Acute LV volume overload due to inter-ventricular volume mismatch is believed by most authors to be the cause for this phenomenon. Another plausible physiopathologic explanation is the acute increase in "wall stress" (Laplace's law) due to acute distention of the cardiac chambers secondary to a sudden increase in venous return at high filling pressures, combined with a "vacuum" effect of the evacuated pericardial space. [source]

Acute and long-term changes in the mesolimbic dopamine pathway after systemic or local single nicotine injections

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2002
R. Ferrari
Abstract We have examined several neurochemical and behavioural parameters related to the function of the mesolimbic dopamine (DA) pathway in animals treated with nicotine following three modes of drug administration, i.e. systemic intraperitoneal injection, intra-accumbens (Acb) infusion or intraventral tegmental area (intra-VTA) microinjection. The present modes of systemic, intra-Acb and intra-VTA nicotine administration elicited comparable acute increases in dialysate DA levels from the Acb. The increase in extracellular DA levels was paralleled by a significant enhancement of locomotion in a habituated environment in the case of systemic or intra-VTA nicotine administration, whereas unilateral or bilateral intra-Acb nicotine infusion was ineffective, showing that accumbal DA increase is not sufficient to elicit locomotion in this experimental paradigm. Intra-VTA, but not systemic or intra-Acb, nicotine administration caused a long-term (at least 24-h) increase in basal dialysate DA levels from the Acb. In addition, significant increases in tyrosine hydroxylase (TH) and GluR1 (but not dopamine transporter or NR1) mRNA levels in the VTA were detected 24 h after intra-VTA nicotine administration. Systemic nicotine injection caused only an increase in TH mRNA levels while intra-Acb infusion did not modify any of the mRNAs tested. The long-term increase in basal DA levels in the Acb and TH, and GluR1 mRNA levels in the VTA upon intra-VTA nicotine microinjection indicates that even a single nicotine injection can induce plastic changes of the mesolimbic DA pathway. [source]

Delirious episodes induced by intravenous administration of clomipramine associated with an acute increase in its plasma concentrations

Reversal Blood Flow Component as Determinant of the Arterial Functional Capability: Theoretical Implications in Physiological and Therapeutic Conditions

ARTIFICIAL ORGANS, Issue 3 2009
Daniel Bia
Abstract In several physiological, pathological, and therapeutic circumstances, the arterial blood flow is acutely modified, increasing, in some vascular segments the reversal (SSR) and oscillatory (SSO) components of the shear stress. Recently, in an in vivo model we found a relationship between acute changes in SSR and SSO, and variations in the arterial viscoelasticity. As the arterial viscoelasticity and diameter are the main determinants of the arterial buffering (BF) and conduit (CF) functions, changes in those functions could be expected associated with variations in SSR and SSO. The aim was to analyze the association between acute increases in SSR and SSO, and changes in the aortic CF and BF. Aortic flow, pressure, and diameter were measured in 16 sheep under basal and high reversal and oscillatory flow conditions (high SSR and SSO). Aortic BF and CF were quantified, and their potential association with the SSR and SSO components were analyzed. During high reversal flow rate conditions, a smooth muscle contraction-pattern was evidenced, with an increase in BF and a decrease in CF. Changes in BF and CF were associated with the changes in SSR and SSO. The acute effects on the arterial wall biomechanics of variations in SSR and SSO could contribute to comprehend their chronic effects, and the meaning of the acute vascular effects of changes in SSR and SSO would depend on the situation. Increases in SSR and SSO could be associated with smooth muscle tone increase-dependent changes in arterial BF and CF. [source]

Endothelium-dependent contractions in hypertension

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2005
Paul M Vanhoutte
1Endothelial cells, under given circumstances, can initiate contraction (constriction) of the vascular smooth muscle cells that surround them. Such endothelium-dependent, acute increases in contractile tone can be due to the withdrawal of the production of nitric oxide, to the production of vasoconstrictor peptides (angiotensin II, endothelin-1), to the formation of oxygen-derived free radicals (superoxide anions) and/or the release of vasoconstrictor metabolites of arachidonic acid. The latter have been termed endothelium-derived contracting factor (EDCF) as they can contribute to moment-to-moment changes in contractile activity of the underlying vascular smooth muscle cells. 2To judge from animal experiments, EDCF-mediated responses are exacerbated by aging, spontaneous hypertension and diabetes. 3To judge from human studies, they contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. 4Since EDCF causes vasoconstriction by activation of the TP-receptors on the vascular smooth muscle cells, selective antagonists at these receptors prevent endothelium-dependent contractions, and curtail the endothelial dysfunction in hypertension and diabetes. British Journal of Pharmacology (2005) 144, 449,458. doi:10.1038/sj.bjp.0706042 [source]