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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma concentrations of arginine-vasopressin (antidiuretic hormone) have been measured in 40 patients with benign essential hypertension and 12 patients with malignant-phase hypertension. Values tended to be low in the benign phase and high in the malignant phase. 5 normal subjects were infused with synthetic arginine-vasopressin, producing plasma concentrations up to five times the highest value recorded in malignant-phase hypertension, without any effect on blood-pressure. There is no evidence that vasopressin has a direct role in the pathogenesis of benign essential hypertension or its transition to the malignant phase. On the contrary, abnormal vasopressin concentrations may be caused by hypertension.
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PMID:Changes of vasopressin in hypertension: Cause or effect? 7 91

The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
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PMID:Formation and action of prostaglandins in the kidney. 53 77

A central stimulatory effect of angiotensin II (AII) on the secretion of arginine-vasopressin (AVP) has been described. The competitive blocker of AII, saralasin (SAR) has been used for diagnostic purposes in angiotensin-dependent hypertension. In addition SAR has a partially agnoistic effect. The aim of the present study was to demonstrate whether AVP-levels can be influenced during SAR-induced renin stimulation. In 9 patients with essential hypertension blood pressure dropped significantly under SAR (10 microgram/kg/min over a 30 min period). Before and after SAR plasma renin activity (PRA) and AVP were measured by RIA, SAR evoked significantly increments of PRA in all patients and of AVP in 6 patients. The increased serum concentrations of AVP following SAR may be explained either by the depressor effect of SAR, its diminished concentration at the central receptor, or a partial AII-agonistic effect.
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PMID:[Effect of saralasin on plasma renin activity and arginine-vasopressin in patients with angiotensin-dependent hypertension (author's transl)]. 68 28

1. The rate of renal excretion of arginine-vasopressin was determined during unrestricted fluid intake for 24 h and in response to fluid deprivation for 18 h in nine young men with very mild essential hypertension and compared with that in sixteen normotensive men of similar age. 2. Despite an equivalent osmolar stimulus, excretion of arginine-vasopressin was significantly greater in the reference group than in the reference group. This difference increased progressively with increasing dehydration. 3. We suggest that these findings are mainly due to an increased rate of secretion of arginine-vasopressin in response to mild hydropenia in hypertensive patients and that a moderate increase of release of arginine-vasopressin during periods of fluid deprivation may exert vascular effects and thus influence the perpetuation of hypertension.
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PMID:Increased renal excretion of arginine-vasopressin during mild hydropenia in young men with mild essential benign hypertension. 107 11

Experimental and clinical studies seem to prove that both endogenous opioids and atrial natriuretic peptide (ANP) are involved in blood pressure regulation. This raised the question, whether these two factors are functionally interrelated to each other. We tried to answer this question by assessing plasma ANP levels in 15 patients with II degrees essential hypertension and in 15 healthy subjects under water immersion (WI) conditions. In all subjects two WI tests were performed--one without pretreatment with naloxone, and a second one after blockade of opioid receptors by this opioid receptor antagonist. Parallel to ANP, plasma renin activity (PRA), aldosterone (ALD) and vasopressin (AVP) were assessed. In hypertensive patients significantly higher basal plasma ANP levels were found than in control subjects. WI induced a significant increase of plasma ANP in both examined groups which became markedly reduced after blockade of opioid receptors by naloxone. Naloxone did not influence the WI induced decrease of PRA, ALD and AVP respectively. From results presented in this study we conclude, that a.) opioid receptors seem to influence regulation of ANP secretion both in healthy normotensive subjects and patients with essential hypertension, and b.) that WI induced alterations of ANP on the one side and of PRA, ALD and AVP on the other side are not interrelated.
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PMID:Do opioid receptors participate in the regulation of atrial natriuretic peptide (ANP) secretion in hypertensive patients? 133 Mar 91

The association of liver cirrhosis with arterial essential hypertension has been previously described. The present study extends the previous reports by investigating the hormonal relationships that may occur in patients with established essential hypertension associated to liver cirrhosis. We studied the renin-angiotensin, the adrenergic systems and other vasoactive hormones such as arginine-vasopressin, atrial natriuretic peptide, endothelin and parathyroid hormone in cirrhotic patients with and without essential hypertension. The data suggested that the coincidence of arterial hypertension in cirrhotic patients was characterized by the following findings: a decreased renin-angiotensin activity; a reduced systemic vasodilatation; an increased peripheral pressor effect of vasoactive hormones and an increased effective blood volume.
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PMID:Hormonal aspects of the relation of liver cirrhosis to essential hypertension. 139 76

The demonstration that exogenous atrial natriuretic polypeptide (ANP) has markedly lowered plasma antidiuretic hormone (ADH) suggests a possible negative control of endogenous ANP on the secretion of ADH from the posterior hypophysis. To test this possibility and to clarify the role of ADH and ANP in the pathophysiology of essential hypertension (EHT), the responses of ADH and ANP to a hypertonic saline infusion were investigated in EHT patients and normotensive subjects (NT). Twenty inpatients with EHT (10 males and 10 females; 50.5 +/- 6.5y) and 10 NT subjects (5 males and 5 females; 50.6 +/- 7.8y) underwent a 20 min intravenous infusion of hypertonic saline (2.5% NaCl; 0.25ml/kg/min) in a fasting state. Blood samples were drawn before and 10, 20, 30, 45 and 60 min after the infusion and analyzed for ADH and ANP as well as plasma osmolarity (Posm), Na and albumin. Basal levels of ADH and ANP were not significantly different between NT and EHT. ADH was rapidly increased by the infusion in both groups; however, its percent increase was much higher in EHT than in NT during and after the infusion. Surprisingly, a highly significant negative correlation between ADH and ANP was found before and after the infusion in both groups. Although blood pressure was not changed significantly, the enhanced response of ADH to a sodium and volume load may play a role in part in the pathophysiology of EHT. In addition, it has been suggested that a possible suppression by ANP on the secretion of ADH may be one of the mechanisms of the diuretic action of ANP.
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PMID:[Responses of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP) to hypertonic saline infusion in essential hypertensive patients and normotensive subjects]. 153 98

To investigate the time course of the effects of alcohol on blood pressure, we studied the response of ambulatory blood pressure, neurohumoral variables, and hemodynamics to a single moderate dose of alcohol in hypertensive patients. Sixteen Japanese men (22-70 years old) with essential hypertension who were habitual drinkers were examined under standardized conditions. On the alcohol intake day, they ingested 1 ml/kg ethanol (vodka) at dinner, and on the control day they consumed a nonalcoholic beverage. The order of the two periods was randomized. Mean ambulatory blood pressure was lower in the alcohol intake period than in the control period (125 +/- 3/74 +/- 2 versus 132 +/- 4/78 +/- 2 mm Hg, p less than 0.05), and the significant depressor effect of alcohol lasted for up to 8 hours after drinking. Blood pressure on the next day did not differ with or without alcohol intake. The acute hypotensive effect of alcohol was associated with an increase in heart rate and cardiac output and with a decrease in systemic vascular resistance as determined by echocardiography. Plasma catecholamine levels and renin activity rose significantly at 2 hours after dinner, whereas vasopressin and potassium levels fell on the alcohol day. Blood glucose and serum insulin levels were comparable between the two periods. Three patients with marked alcohol-induced flush had greater hypotensive and tachycardiac responses than those who did not show an alcohol-induced flush. The change in mean blood pressure induced by alcohol was negatively correlated with age, the baseline blood pressure, and the change in plasma norepinephrine. These results indicate that the major effect of acute alcohol intake is to lower blood pressure through systemic vasodilatation in hypertensive subjects. Ambulatory blood pressure monitoring may be useful for assessing blood pressure in habitual drinkers.
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PMID:Acute depressor effect of alcohol in patients with essential hypertension. 163 64

A group of consecutive 180 veteran patients with mild to moderate essential hypertension were chosen to participate in clinical antihypertensive trial for the purpose of defining the role of converting enzyme inhibitors and renin-angiotensin-aldosterone system in the management of mild to moderate hypertension patients. After a two-week placebo period, these patients were randomly assigned to regimens of converting enzyme inhibitors (enalapril or captopril with or without diuretics) or conventional therapy (diuretics with or without traditional vasodilators with or without beta-blockers). Each patient was regularly followed up every two weeks and doses were added until the diastolic blood pressure was equal to or lower than 90 mmHg. After 1 year of follow-up, only 162 patients completed the study. All high blood pressure was significantly reduced by these three regimens, but no significant difference of blood pressure control was noted. The mean left ventricular ejection fraction increased from 55.9 +/- 6.2 to 57.5 +/- 5.3% in captopril group (P less than 0.05, n = 59) and from 54.8 +/- 6.8 to 57.2 +/- 5.8% enalapril group (P less than 0.01, n = 53), in contrast to the insignificant change in control group (n = 50) (56.5 +/- 7.7 to 56.6 +/- 5.9%). The exercise duration also significantly increased only in converting enzyme inhibitors group (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.01). Furthermore, the plasma aldosterone level was significantly reduced by converting enzyme inhibitors therapy, whereas conventional therapy had no beneficial effect (P less than 0.001). Concomitantly, antidiuretic hormone and plasma norepinephrine levels were also significantly reduced by converting enzyme inhibitors. In addition, converting enzyme inhibitors had a favorable trend to affect the metabolism of lipid in contrast to the conventional therapy. These results show that a first-step treatment of hypertension with converting enzyme inhibitors permits better left ventricular function and improves exercise tolerance by way of renin-angiotensin-aldosterone system inhibition. Thus, converting enzyme inhibitors might be suggested as the first step regimen in the treatment of hypertension.
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PMID:Comparisons of long-term effects between converting enzyme inhibitors and conventional therapy in treating mild to moderate hypertension. 165 34

In the first part of the text the main elements of renal physiology are mentioned as well as the role played by sodium-modulating hormones in the preservation of sodium and water homeostasis. A personal contribution concerns the release as well as the circadian rhythm of atrial natriuretic peptide (ANP) and of the digitalis-like substance (DLS). In the second part, the problem is dealt with from a pathophysiologic point of view, with reference made to the literature, and to our own data. In particular, the problem of essential hypertension with reduced levels of plasma renin activity (PRA) is thoroughly analyzed. As is well known, this kind of hypertension is characterized by normal plasma aldosterone levels associated with reduced kallikrein urinary excretion. The data we gathered not only confirmed these findings but also enabled us to point out other typical features of this particular kind of hypertension: normal values of vasopressin, elevation of ANP and DLS, hyperactivity of Na+/K+ cotransport. The introduction of a single variant in the sodium-modulating systems confirmed that the low PRA patient also behaves distinctively from a dynamic point of view. In fact, prostaglandin inhibition determines hypertension only in these patients, while both oral kallikrein administration and intravenous ANP administration were particularly effective because of a primitive deficit of the natriuretic paracrine systems paralleled by a compensatory increase of ANP. After identifying this group of hypertensive patients we intended to ascertain whether, even in the normal or high PRA patients, it was possible to identify a sub-group of subjects with altered sodium-modulation. The patients we examined were subdivided according to their hormonal and renal response to a saline load, and to angiotensin II, into "modulators" (with normal) and "nonmodulators" (with reduced sodium excretion capacity). An analysis of the hormonal characteristics of non-modulators identified an increased responsiveness of all sodium-modulation systems and not only of the renin-angiotensin-aldosterone system as pointed out by some other authors. The last part of the text is devoted to clinical and therapeutic problems. The behaviour of the daily blood pressure profile in patients with essential hypertension, and then the influence that sodium-modulating systems may have on pressure are discussed. The consequences of a progressive reduction in renal function on the circadian rhythm of arterial pressure are then assessed, and, at the same time, how renal impairment parallels the flattening of the daily pressure rate is observed.
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PMID:The kidney and essential hypertension. 183 73


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