Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to determine plasma endothelin-1 levels in patients with essential hypertension and diabetes mellitus. Endothelin immunoreactivity was measured in normal controls (n = 30), mild-moderate essential hypertensives (n = 25), Type II diabetic normotensives (n = 25) and hypertensive patients (n = 20). In addition, in ten patients of each group we investigated the relationships of endothelin with other vasoactive hormones. Plasma endothelin concentrations were similar in healthy controls, in essential hypertensives and in diabetic patients with or without hypertension, averaging 8.23 +/- 1.68 pg/ml, 7.7 +/- 1.1 pg/ml, 5.05 +/- 0.94 pg/ml, 7.88 +/- 1.41 pg/ml, respectively. No correlations were observed between endothelin and concentrations of plasma renin activity, aldosterone, catecholamines, atrial natriuretic peptide and arginine-vasopressin. The present study suggests that Type II diabetic patients with or without essential hypertension do not have demonstrably higher values of plasma endothelin than essential hypertensives or healthy subjects.
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PMID:Plasma endothelin in essential hypertension and diabetes mellitus. 841 Sep 22

The early stages of weight loss are associated with a reduction in blood pressure, and the mechanisms mediating this reduction remain unclear. Platelet free calcium levels, [Ca2+]i, have been reported to be elevated in essential hypertension and to decrease with pharmacological treatment of the hypertension. In the current study, 18 obese subjects had measurements of blood pressure, forearm blood flow, forearm vascular resistance, and both basal platelet [Ca2+]i and [Ca2+]i responses to vasopressin during 12 weeks on a very low calorie (3,360 kJ, or 800 kcal) diet. Weight reduction was associated with reduction in mean arterial blood pressure at 3-4 weeks. There were associated reductions in forearm vascular resistance and platelet [Ca2+]i as well as increases in forearm blood flow at 3-4 weeks of the diet. Increased forearm blood flow was correlated with weight loss. Vasopressin-induced platelet [Ca2+]i responses increased, which correlated with the reduction in mean arterial pressure at 7-8 weeks of weight loss. Assuming that platelet [Ca2+]i metabolism reflects vascular smooth muscle cell [Ca2+]i metabolism, the data suggest that blood pressure reduction after weight loss may be related to reduced vascular smooth muscle cell [Ca2+]i. The reason for the increased vasopressin-induced [Ca2+]i after weight reduction is unclear.
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PMID:Effects of weight reduction on cellular cation metabolism and vascular resistance. 847 40

In this study we investigated, by means of the spectral analysis approach, the possible alterations in the activity of the pressor-control mechanisms in relation to the development of essential hypertension. Since the maintenance of controlled arterial blood pressure (ABP) levels is achieved by a continuously fluctuating control system, instantaneous ABP varies continuously in direct correlation with the activation of various control branches. The power spectrum of ABP fluctuations thus provides a quantitative measure of the activity of the various controlling mechanisms. Two strains of rats, Spontaneously Hypertensive Rats (SHR) and Wistar-Kyoto normotensive rats (WKY), were subjected to acute hemorrhage, a procedure known to trigger a strong response, of both the neural (autonomic nervous system) and the hormonal (renin-angiotensin and vasopressin) systems. ABP was continuously recorded from the caudal artery in conscious, 1-month-old SHR and WKY. Three groups of rats were studied. Group 1, acute 2-ml hemorrhage; Groups 2, injection of prazosin (2.5 mg/kg) or Group 3, captopril (4 mg/kg), each followed by bleeding as in the group 1. Spectral analysis of ABP fluctuations was performed on time traces of 20 min duration. The low-frequency part of the power spectrum was analyzed. Three frequency bands were investigated: 0.004-0.04 Hz, 0.04-0.07 Hz and 0.07-0.1 Hz. In SHR, although the baseline mean ABP levels were similar to those of WKY, ABP fluctuations were significantly dampened in SHR in each of the three frequency ranges. Hemorrhage induced, in both strains, a similar fall in mean ABP accompanied by an increase in the slow ABP fluctuations. However, in SHR, the response was significantly greater that that of WKY. The steepest response was observed in the slowest, 0.004-0.04 Hz frequency band, 8.7 +/- 1.7 vs. 1.5 +/- 0.4 times the baseline levels. However, this intense increase in power after hemorrhage brought the two strains to similar levels. The difference in the response to bleeding was eliminated, in the three frequency ranges, by alpha 1 blockade. Captopril reduced the response to bleeding in SHR, to the level observed in WKY in all three frequency bands. Spectral analysis of the spontaneous oscillations in ABP unmasks abnormalities which conventional blood pressure measurements cannot detect in 1-month-old, still normotensive SHR. It thus, provides a tool to study the dynamics of the abnormalities which precede the development of hypertension. Bleeding amplifies the malfunction observed in SHR under baseline conditions, since the mean ABP levels were similar in both strains before and after bleeding, SHR seem to retain the ability to respond to a fall in blood volume by requiring a greater recruitment of the control mechanisms than WKY.
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PMID:Insight into blood-pressure control in SHR via the response to acute hemorrhage: a spectral analysis approach. 880 Dec 64

We assessed various aspects of endocrine function in patients treated for essential hypertension with manidipine chloride, a calcium channel blocker, to study the effects of this drug on several endogenous humoral factors, including human atrial natriuretic peptide (hANP) and endothelin 1 (ET), which influence vasoconstriction and blood fluid volume. The study included 19 patients with essential hypertension. All patients received manidipine chloride 10 mg/d for 24 weeks. After treatment blood pressure was normalized in all patients, and there were no significant changes in plasma renin activity or blood concentrations of vasopressin, hANP, ET, aldosterone, adrenaline, or noradrenaline. There was a statistically significant negative correlation between the change in ET levels and hANP levels before and after treatment. We also observed a statistically significant negative correlation between the change in systolic blood pressure caused by manidipine chloride and the change in hANP levels before and after treatment. These findings suggest that hANP and ET levels are systematically changed by manidipine chloride in patients with essential hypertension. We also speculate that changes in blood pressure may be closely related to levels of hANP in patients treated with manidipine chloride.
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PMID:Effect of manidipine chloride on various aspects of endocrine function, including plasma levels of endothelin-1 and human atrial natriuretic peptide, in patients with essential hypertension. 887 96

Individuals with essential hypertension have been characterized by increased renal sympathetic vascular tone with decreased plasma volume and normal cardiac output compared with normotensive individuals. We used a servo-controlled intrarenal infusion system to evaluate the hemodynamic, renal excretory, and plasma hormonal responses to 28-day, low-level elevations in the intrarenal adrenergic neurotransmitter norepinephrine. In uninephrectomized dogs (n = 6), servo-controlled norepinephrine infusion increased mean arterial pressure from 95.6 +/- 3.1 to 115.7 +/- 4.9 mm Hg on day 1 without concomitant reductions in renal blood flow. Arterial hypertension was sustained and renal vascular resistance increased during the 28 days of servo-controlled norepinephrine infusion despite significant decreases in the daily dose of intrarenal norepinephrine (1.49 +/- 0.23 to 0.47 +/- 0.25 mg/d) necessary to maintain renal blood flow constant. Arterial pressure returned to control values with the cessation of servo-controlled norepinephrine, whereas renal blood flow and renal vascular resistance remained slightly decreased and increased, respectively. Cumulative sodium balance exhibited a net 177 +/- 37 mmol sodium loss over the 28 days of norepinephrine infusion, indicating that the hypertension did not result from sodium retention or expansion of extracellular fluid volume. Intrarenal norepinephrine did not change plasma epinephrine, norepinephrine, or vasopressin concentrations. Atrial natriuretic factor, however, increased at 7 and 14 days of servo-controlled norepinephrine, and plasma renin activity increased on day 14 of norepinephrine infusion. We conclude that low-level elevation of intrarenal adrenergic neurotransmitter produces sustained arterial hypertension that is independent of expansion in extracellular fluid volume, increases in circulating catecholamines or plasma renin activity, or reductions in renal blood flow. This hypertension may be associated with increased renal vascular sensitivity to norepinephrine and/or other renal vasoactive factors.
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PMID:Chronic renal neuroadrenergic hypertension is associated with increased renal norepinephrine sensitivity and volume contraction. 895 93

The use of diuretics leads to a negative sodium and fluid balance without primary effects on serum sodium concentration. This parameter is regulated by the activity of the antidiuretic hormone (ADH) system. Secondary changes in other electrolyte systems and in acid base homeostasis also are induced by diuretic therapy. Especially diuretic induced hypokalemia is important as it is responsible for the excess mortality observed in patients with diuretic treated essential hypertension and cardiac abnormalities. All adverse metabolic effects of diuretic therapy are, in contrast to the antihypertensive action, dose dependent. Changes in fluid and electrolyte metabolism induced by diuretics occur within the first 2 or 3 weeks after initiation of medication. Counterregulatory mechanisms are activated and a new steady state is established. Serial laboratory determinations after this period are not necessary as long as this steady state is not affected by additional events (like a change in therapy or diet as well as the occurrence of vomiting or diarrhea).
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PMID:[Effects of diuretic therapy on electrolyte and acid-base homeostasis]. 903 78

To study the role of vasopressin (VP) in essential hypertension, we examined plasma levels of VP and blood pressure (BP) response to an orally active V1 receptor antagonist, OPC-21268, in hypertensive patients on diets with different sodium contents. Plasma VP was determined in 12 normotensive subjects and 12 patients with mild essential hypertension on a regular sodium diet, and in eight hypertensive patients on a high sodium (250 mmol/day) and a low sodium (25 mmol/day) diet. BP response was examined for 4 h after single oral administration of OPC-21268 (100 mg) or placebo in eight patients on the regular diet, and in six patients on the high and low sodium diets. In four patients on the regular diet, the effects of OPC-21268 on the baroreflex control of heart rate were also examined with intravenous injections of methoxamine. Plasma VP did not differ between the normotensive and hypertensive subjects. Levels of VP in the plasma was higher in the high sodium than in the low sodium period, but the difference was not significant. BP and heart rate did not change significantly after administration of OPC-21268 or placebo under either condition. OPC-21268 also failed to lower BP in salt-sensitive patients on the high sodium diet. The baroreceptor reflex sensitivity was not modified by the administration of OPC-21268. Our results suggest that VP does not play an important role in mild essential hypertension through its action on the V1 receptors regardless of dietary sodium intake.
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PMID:The role of vasopressin in essential hypertension. Plasma levels and effects of the V1 receptor antagonist OPC-21268 during different dietary sodium intakes. 939 42

In the last decade, two types of genes participating in the etiology of hypertension have been identified. The primary genes or blood pressure regulators are those that codify enzymes (renin, kallikrein, kininase, aminopeptidase), hormones (angiotensins, vasopressin, aldosterone, prostaglandins, and atrial natriuretic peptide) and substrates (angiotensinogen and kininogen). They cause arteriolar vasodilation or vasoconstriction or sodium retention in the extravascular space. Allelic polymorphisms associated to essential hypertension have been described. The secondary genes are those that produce hereditary diseases of low prevalence, associated to hypertension in 20 to 80% of patients (polycystic kidney disease, pheochromocytoma, adrenal hyperplasia, hereditary nephritis). Forty genes located in all chromosomes, that are dominantly, recessively or X-linked transmitted, have thus far been identified. Chromosomal maps with all genic loci are presented.
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PMID:[The genes of human hypertension]. 946 Feb 75

Suprachiasmatic and paraventricular hypothalamic nuclei (SCN and PVN, respectively) were studied in humans with essential hypertension (EH) and in healthy individuals who had normal blood pressure and died by accident (control group). Immunohistochemistry, hybridization in situ using computer image analysis have shown that EH patients have decreased number of vasopressin (VP) positive cells in SCN, high number of corticotropin-releasing hormone (CRH) producing neurones in PVN and increased amount of mRNA for CRH in them. A negative linear correlation was found between the number of CRH-producing cells in PVN, amount of mRNA for CRH in them and the number of VP-synthesizing cells in SCN. The presence of GABA in VP-producing cells in SCN together with the data obtained suggest the presence of certain "disinhibition" of CRH-producing cells in PVN in EH which could cause enhanced synthesis of ACTH in anterior hypophysis and increased secretion of corticosteroids by the adrenal gland.
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PMID:[Changes in suprachiasmatic and paraventricular hypothalamic nuclei in essential hypertension]. 1047 39

Dopamine modulates cardiovascular function by actions in the central and peripheral nervous system, by altering the secretion/release of prolactin, pro-opiomelanocortin, vasopressin, aldosterone, and renin, and by directly affecting renal function. Dopamine produced by the renal proximal tubule exerts an autocrine/paracrine action via two classes of dopamine receptors, D1-like (D1 and D5) and D2-like (D2, D3, and D4), that are differentially expressed along the nephron. The autocrine/paracrine function of dopamine, manifested by tubular rather than by haemodynamic mechanisms, becomes most evident during extracellular fluid volume expansion. This renal autocrine/paracrine function is lost in essential hypertension and in some animal models of genetic hypertension. The molecular basis for the dopaminergic dysfunction in hypertension may involve an abnormal post-translational modification of dopamine receptors.
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PMID:D1 dopamine receptor signalling defect in spontaneous hypertension. 1069 8


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