Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high salt diet often is regarded as an accessory risk factor in hypertension, coincidental to the deleterious effect of high blood pressure on vasodilator function. The aim of this study was to determine whether short-term ingestion of a high salt diet per se impairs vasodilator function in the cerebral circulation independent of blood pressure changes. Adult Sprague-Dawley rats were fed a normal salt (0.8%) or high salt (4%) diet for 3 days. Mean arterial pressures were similar in the normal and high salt groups (123+/-2 and 125+/-2 mm Hg, respectively). Subsequently, the responses of the in situ pial arterioles to acetylcholine, iloprost, and sodium nitroprusside were determined in cranial windows using intravital videomicroscopy. Pial arterioles of rats fed normal and high salt diets showed similar resting diameters of 69+/-2 and 72+/-3 microm, respectively, but their reactivity patterns to vasodilator stimuli were markedly different. Arterioles of rats fed a normal salt diet dilated progressively up to 17+/-3% in response to the endothelium-dependent agent acetylcholine (10(-9) to 10(-6) mol/L) and dilated by 22+/-2% in response to the prostaglandin I2 receptor agonist iloprost (3x10(-11) mol/L). In contrast, pial arterioles of rats fed a high salt diet constricted by 4+/-3% and 8+/-2% in response to acetylcholine and iloprost, respectively. Sodium nitroprusside (10(-6) mol/L), a nitric oxide donor, dilated pial arterioles of rats fed low and high salt diets by a similar amount (19+/-3% and 16+/-2%, respectively), suggesting that signaling mechanisms for dilation distal to the vascular smooth muscle membrane were intact after high salt intake. These results provide the first evidence that the short-term ingestion of a high salt diet may severely impair the vasodilator function of the in situ cerebral microcirculation independent of blood pressure elevation.
Hypertension 1999 Feb
PMID:Loss of endothelium and receptor-mediated dilation in pial arterioles of rats fed a short-term high salt diet. 1002 28

A 29-year-old man developed acute oliguric renal failure with severe hypertension and microangiopathy. He was treated with hemodialysis and anti-hypertensive drugs, but oliguria was prolonged. A renal biopsy was performed on the 29th hospital day. Small arteries and arterioles were characterized by marked intimal thickening, and most of the glomeruli showed ischemic changes. Although there was extensive tubular loss and atrophy, regenerative changes were occasionally observed in some tubules, in which 90-kDa heat-shock protein was induced. He was diagnosed as having malignant nephrosclerosis, and was treated with a prostaglandin I2 analog, in addition to anti-hypertensive drugs. Thereafter, his renal function recovered gradually, and hemodialysis was discontinued on the 49th hospital day. Functional recovery lasts more than five years. We suggest that the expression of HSP90 in regenerative tubular cells is a useful histological indicator for predicting recovery from acute oliguric renal failure due to malignant hypertension.
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PMID:Expression of 90-kDa heat shock protein within regenerative tubular cells in a patient with acute oliguric renal failure due to malignant hypertension. 1004 23

It is well known that in haemodialysis patients suffering from oligoanuria, extracellular hypervolaemia develops and this hypervolaemia is the main reason for hypertension occurring in some of the patients. The absence of vasorelaxation during hypervolaemia may be secondary to an increased activity of vasoconstrictor systems and/or a decreased formation of vasodilator agents like prostaglandin E2(PGE2) and prostaglandin I2(PGI2). In the present study, arterial PGE2 and leukotriene C4(LTC4)-like activities and the effect of fluid removal on these arachidonic acid metabolites during haemodialysis were measured in normotensive and hypertensive patients. Plasma PGE2 and LTC4-like activities were significantly different between hypertensive and normotensive patients. PGE2/LTC4 ratio did not change in normotensive patients while it was increased in hypertensive patients after haemodialysis. These results indicate that haemodialysis alters the synthesis of arachidonic acid metabolites especially in hypertensive patients.
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PMID:Changes of arterial arachidonic acid metabolites in hypertensive patients during haemodialysis. 1018 68

We investigated the protective effect of chronic treatment with AE0047, a dihydropyridine-type calcium channel blocker, on vascular endothelial abnormalities in stroke-prone spontaneously hypertensive rats (SHRSP). Ten-week repeated antihypertensive treatment with AE0047 inhibited blood pressure elevation and improved endothelium-dependent relaxation in response to acetylcholine in aorta isolated from SHRSP. Furthermore, the abnormal production of prostaglandin I2 and thromboxane A2 in the aorta was normalized to a level equivalent to that in Wistar-Kyoto rats. These results suggest that chronic treatment with AE0047 exerts protective effects against endothelial abnormalities associated with the development of hypertension.
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PMID:Protection against endothelial abnormalities by a novel calcium channel blocker, AE0047, in stroke-prone spontaneously hypertensive rats. 1021 83

It has been suggested that the hypercoagulable state in severe preeclampsia is strongly related to the onset of intrauterine growth retardation (IUGR) through the deterioration of placental circulation. In this study, one of two kinds of anticoagulants, heparin or antithrombin (AT), was given to severe early-onset preeclamptic women (onset before 32 weeks of gestation) with IUGR, and the efficacies in maternal and fetal findings were compared. The mechanism of AT to improve placental circulation was discussed based on our previous study using the culture system of chorionic trophoblastic cells. The mean systolic blood pressure decreased significantly in the AT group (AT concentrate 1,500 IU/d for 7 days, n = 15). Fetal growth was calculated by ultrasonographic measurement, and the weight gain was higher in the AT group than it was in the heparin group. In vitro experiments showed that AT increased the thrombomodulin (TM) antigen on the cell surface and also increased prostaglandin I2 (PGI2) production by cultured trophoblastic cells. This suggests that AT replacement therapy is useful for improving maternal hypertension and fetal findings in severe preeclampsia with IUGR through the increase of TM and PGI2 production in both maternal and placental circulation.
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PMID:Efficacy of antithrombin replacement therapy in severe early-onset preeclampsia. 1062 3

Renal cyclooxygenase-1 and cyclooxygenase-2 actively metabolize arachidonate to metabolism five primary prostanoids: prostaglandin E2, prostaglandin F2a, prostaglandin I2, thromboxane A2, and prostaglandin D2. These lipid mediators interact with a family of distinct G-protein-coupled prostanoid receptors designated EP, FP, IP, TP, and DP, respectively, which exert important regulatory effects on renal function. The intrarenal distribution of these prostanoid receptors has been mapped and the consequences their activation are being characterized. The FP, TP, and EP1 receptors preferentially couple to increased cell Ca2+. EP2, EP4, DP, and IP receptors stimulate cyclic adenosine monophosphate, whereas the EP3 receptor preferentially couples to Gi, inhibiting cyclic adenosine monophosphate generation. EP1 and EP3 messenger RNA expression predominate in the collecting duct and thick limb, respectively, where their stimulation reduces sodium chloride and water absorption, promoting natriuresis and diuresis. Interestingly, only a mild change in renal water handling is seen in the EP3 receptor knockout mouse. Although only low levels EP2 receptor messenger RNA are detected in kidney and its precise intrarenal localization is uncertain, mice with targeted disruption of the EP2 receptor display salt-sensitive hypertension, suggesting it also plays an important role in salt excretion. In contrast, EP4 messenger RNA is readily detected in the glomerulus where it may contribute to the regulation of renin release and decrease glomerular resistance. TP receptors are also highly expressed in the glomerulus, where they may increase glomerular vascular resistance. The IP receptor messenger RNA is most highly expressed in the afferent arteriole and it may also modulate renal arterial resistance and renin release. At present there is little evidence for DP receptor expression in the kidney. Together these receptors act as physiologic buffers that protect the kidney from excessive functional changes during periods of physiologic stress. Loss of the combined effects of these receptors contributes to the side effects seen in the setting of nonsteroidal anti-inflammatory drug administration, whereas selective antagonists for these receptors may provide new therapeutic approaches in disease.
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PMID:Prostaglandin receptors: their role in regulating renal function. 1065 21

This study was designed to examine the contribution of lipoxygenase products to mechanisms of vascular contraction and elevated blood pressure in rats with aortic coarctation-induced hypertension. In cytosolic fractions of aortae taken from hypertensive rats, 12-lipoxygenase protein was increased as compared to normotensive controls. Aortic rings from hypertensive, but not from normotensive rats, exhibited a basal tone which was reduced 74+/-12 and 71+/-22%, respectively, by the lipoxygenase inhibitors cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (CDC, 10(-5) mol/L) and 5,8,11-eicosatriynoic acid (ETI, 10(-5) mol/L). CDC (8 mg/kg s.c.) did not affect the blood pressure of normotensive rats but decreased that of hypertensive rats from 182+/-6 to 151+/-10 mm Hg. The blood pressure lowering effect of CDC was blunted in hypertensive rats pretreated with indomethacin or antibodies against 5,6-dihydro-prostaglandin I2. These data suggest contribution of lipoxygenase-derived products to mechanisms underlying aortic smooth muscle basal tone and elevated blood pressure in rats with aortic coarctation-induced hypertension. The vasodepressor effect of CDC depends on a mechanism involving vasodilatory prostaglandins.
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PMID:Lipoxygenase-dependent mechanisms in hypertension. 1074 58

Pulmonary hypertension is a pathologic condition characterized by elevated pulmonary artery pressures and an associated vasculopathy. Primary pulmonary hypertension (PPH) is a rare condition with a sporadic occurrence and a familial form of the disorder. Abnormal vasomotor tone in the pulmonary vasculature results from an imbalance of the action of various vasoconstrictors/ vascular proliferative agents (endothelin and thromboxane) versus vasodilators /anti-proliferative agents (prostacyclin and nitric oxide). The mainstay of outpatient therapy has been the use of digitalis, diuretics, oxygen, and coumadin and the judicious use of vasodilator therapy. Calcium channel blockers in a select group and intravenous prostacyclin have dramatically improved survival for those with primary pulmonary hypertension. Use of prostaglandin I2 (PGI2) in other forms of chronic pulmonary arterial hypertension is not as clear, although evidence of initial beneficial response is promising. Importantly, over the next few years both pharmacologic and nonpharmacologic treatment modalities for pulmonary hypertension may rapidly change as we focus more on the abnormal pulmonary vascular biology and concomitant hemodynamic and neurohormonal milieu.
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PMID:Current management of patients with pulmonary hypertension and right ventricular insufficiency. 1098 Aug 99

Renal cyclooxygenase 1 and 2 activity produces five primary prostanoids: prostaglandin E2, prostaglandin F2alpha, prostaglandin I2, thromboxane A2, and prostaglandin D2. These lipid mediators interact with a family of distinct G protein-coupled prostanoid receptors designated EP, FP, IP, TP, and DP, respectively, which exert important regulatory effects on renal function. The intrarenal distribution of these prostanoid receptors has been mapped, and the consequences of their activation have been partially characterized. FP, TP, and EP1 receptors preferentially couple to an increase in cell calcium. EP2, EP4, DP, and IP receptors stimulate cyclic AMP, whereas the EP3 receptor preferentially couples to Gi, inhibiting cyclic AMP generation. EP1 and EP3 mRNA expression predominates in the collecting duct and thick limb, respectively, where their stimulation reduces NaCl and water absorption, promoting natriuresis and diuresis. The FP receptor is highly expressed in the distal convoluted tubule, where it may have a distinct effect on renal salt transport. Although only low levels of EP2 receptor mRNA are detected in the kidney and its precise intrarenal localization is uncertain, mice with targeted disruption of the EP2 receptor exhibit salt-sensitive hypertension, suggesting that this receptor may also play an important role in salt excretion. In contrast, EP4 receptor mRNA is predominantly expressed in the glomerulus, where it may contribute to the regulation of glomerular hemodynamics and renin release. The IP receptor mRNA is highly expressed near the glomerulus, in the afferent arteriole, where it may also dilate renal arterioles and stimulate renin release. Conversely, TP receptors in the glomerulus may counteract the effects of these dilator prostanoids and increase glomerular resistance. At present there is little evidence for DP receptor expression in the kidney. These receptors act in a concerted fashion as physiological buffers, protecting the kidney from excessive functional changes during periods of physiological stress. Nonsteroidal anti-inflammatory drug (NSAID)-mediated cyclooxygenase inhibition results in the loss of these combined effects, which contributes to their renal effects. Selective prostanoid receptor antagonists may provide new therapeutic approaches for specific disease states.
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PMID:G protein-coupled prostanoid receptors and the kidney. 1118 68

Chronic administration of erythropoietin (EPO) is often associated with hypertension in animals and humans. The aim of this study was to estimate whether 1-week treatment with EPO can affect the vascular endothelial function. Rabbits were given with EPO (400 iu kg(-1) s.c.) or saline each other day for 1 week. Hypotensive responses to intravenously given acetylcholine (ACh), endothelium-independent nitric oxide donors (NOC7, nitroprusside and nitroglycerin) and prostaglandin I2 were tested before and after administration of N(G)-nitro-L-arginine methyl ester (L-NAME), a specific nitric oxide synthase inhibitor, under pentobarbitone anaesthesia. Blood haemoglobin concentration in EPO group was significantly higher than that in control group, whereas baseline values of aortic pressure, heart rate and femoral vascular resistance were similar. The dose of ACh (172 ng kg(-1)) requiring for a 15 mmHg hypotension from the baseline in EPO group was apparently higher than that (55 ng kg(-1)) in control group. On the contrary, hypotensive responses to NOC7, nitroprusside, nitroglycerin and prostaglandin I2 were comparable between two groups. The extent of ACh-induced hypotension did not correlate with haemoglobin concentration. L-NAME significantly inhibited the ACh-induced vasodilating response in control group but did not in EPO group. In another set of rabbits, the same treatment with EPO also decreased vasodilating responses to carbachol, bradykinin and substance P besides ACh as compared with control group. These results indicate that 1-week treatment with EPO selectively attenuates depressor responses to endothelium-dependent vasodilators in anaesthetized rabbits, most likely due to inhibition of endothelial nitric oxide synthase.
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PMID:Effect of 1-week treatment with erythropoietin on the vascular endothelial function in anaesthetized rabbits. 1137 56


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