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

Plasma vasopressin levels were compared in three groups comprising normotensive, mildly hypertensive, and more severely hypertensive patients, both under basal conditions and following an 85 degrees head-up tilt, a stimulus known to provoke vasopressin release in man. Vasopressin levels increased two- to fivefold in all subjects after tilt; however, neither the basal levels nor the maximal levels attained at 45 to 60 minutes after tilt differed in the three groups. These data do not support the postulated role for vasopressin in the causation or perpetuation of non-accelerated essential hypertension in man.
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PMID:Plasma vasopressin and blood pressure. Studies in normal subjects and in benign essential hypertension at rest and after postural challenge. 684 15

In a single-dose crossover study Captopril (SQ 14225), 1 mg/kg body weight, and Nifedipine (Bay a 1040) 20 mg were administered orally to 12 hospitalized patients with essential hypertension (Stage 1 or 2, W.H.O.). Both drugs significantly reduced blood pressure, but each dose acted differently: the mean maximum arterial pressure reduction was faster and greater with Nifedipine than with Captopril: -23 +/- 2% at 37 +/- 15 min and -17 +/- 1% at 86 +/- 25 min, respectively. Captopril inhibited angiotensin II and aldosterone production, but did not accelerate heart rate or stimulate vasopressin release. Nifedipine stimulated vasopressin release and increased heart rate, but the renin angiotensin aldosterone system was not significantly affected. The blood pressure reduction was related to the initial level of activation of the renin angiotensin system only for Captopril. The blood pressure reduction induced by one drug was not related to that produced by the other in the same patient.
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PMID:Antihypertensive and hormonal effects of single oral doses of captopril and nifedipine in essential hypertension. 702 55

The contribution of vasopressin to the hypertensive process has been examined in a number of models of hypertension. Vasopressin is essential for the production of DOC-salt hypertension in the rat, It is likely that vasopressin is required in the early stages of this model of hypertension for its antidiuretic activity and contributes to the later stages of the hypertension as a pressor agent. Vasopressin secretion is increased in SHR, but there may be some differences between the SHR and stroke-prone SHR strains. The pressor action of vasopressin appears to be important in the stroke-prone SHR with well-established hypertension, but not in the young SHR. Vasopressin secretion is greater in Dahl S rats on a high salt diet than in similarly treated R rats. Blockade of vasopressin's pressor activity failed to lower blood pressure in these S rats, unless they were pretreated with captopril. There is insufficient information to determine whether vasopressin has a role in the hypertension in NZGH rats. Vasopressin appears to function as a pressor agent in some, but not all, rats with two-kidney, one clip hypertension. Although vasopressin is not essential for the production of one-kidney, one clip hypertension, it apparently contributes to the hypertension by virtue of its antidiuretic activity. Vasopressin secretion is elevated in partial nephrectomy-salt hypertension, and here, too, it is needed for its antidiuretic action. The question of whether vasopressin secretion is elevated in human essential hypertension is controversial, and its role remains to be determined.
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PMID:Contribution of vasopressin to hypertension. 704 34

In patients with essential hypertension the blood antidiuretic activity was studied in relation to the haemodynamics. It was found that the blood antidiuretic activity increased in parallel with the rise in the total peripheral resistance, and with the decreases in the blood and plasma volumes, stroke volume, and end-diastolic heart volume. The role of antidiuretic hormone in the regulation of haemodynamics in hypertensive patients is discussed.
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PMID:Blood antidiuretic activity and selected haemodynamic indicators in patients with essential hypertension. 739 48

The effects of high and low salt diet on exaggerated natriuresis after volume expansion were examined in two groups of hypertensive patients, 6 with labile and 6 with fixed uncomplicated essential hypertension. Fixed hypertensives eliminated the administered salt-load faster than the labile hypertensives, and diet had no effect on the exaggerated natriuresis of both groups. No association was observed between plasma renin activity and natriuresis in both groups of patients. We conclude that, 1) diet did not affect the saline-induced natriuresis in hypertensive patients, 2) there was no apparent association between plasma renin activity and exaggerated natriuresis in hypertension, 3) other factors such as the capacitance system and vasopressin may play an important role in volume expansion natriuresis, especially in fixed hypertensives.
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PMID:Effects of diet on exaggerated natriuresis in hypertension. 747 92

To appreciate the role of some neuropeptides in the antihypertensive mechanism of clonidine, 17 patients with essential hypertension were given po clonidine 150 micrograms tid for 3 d. Plasma atrial natriuretic factor (ANF), vasopressin (Vas), and dynorphin A (Dyn A) were measured by radioimmunoassay. After the treatment, mean blood pressure (MBP), heart rate and 24 h urine norepinephrine, epinephrine were decreased, but no change was found in plasma Dyn A. The magnitudes of increased ANF and decreased Vas were correlated with the decreased MBP (r = -0.57 and 0.53, respectively, P < 0.05). These results suggest that both ANF and Vas are involved in the antihypertensive mechanism of clonidine.
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PMID:[Possible involvement of atrial natriuretic factor and vasopressin in antihypertensive mechanism of clonidine in humans]. 790 63

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension. 795 85

Measurements of blood lipids and hormones (plasma renin, aldosterone, vasopressin, prolactin, atrial natriuretic peptide, beta-endorphin, thyrotropin, thyroid hormones) in two groups of patients suffering from obesity (group 1: 64 patients with arterial hypertension and group 2: 26 patients with normal arterial pressure) have brought the authors to a conclusion that arterial hypertension in young obese patients is an early manifestation of essential hypertension. Hormonal dysfunction in obese patients is conducive to early development of essential hypertension in cases when there is a hereditary predisposition to it.
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PMID:[Hormonal aspects of the pathogenesis of arterial hypertension in young obese patients]. 810 42

The levels of plasma arginine-vasopressin (AVP) in 80 patients with essential hypertension were measured, and its impact on the disease and its clinical significance were studied. The results showed that: (1) The levels of plasma AVP in patients with essential hypertension were significantly higher than that in normotensive subjects (P < 0.001). It dropped to normal level after antihypertensive drugs. (2) The concentrations of plasma AVP in both hypertensive subjects and normotensive subjects were not correlated with age and sex (P < 0.05). (3) The concentration of plasma AVP in patients with essential hypertension was the highest in stage III, the lowest in stage I, and middle in stage II. (4) The levels of plasma AVP in patients with malignant hypertension were significantly higher than that in patients with benign hypertension (P < 0.05). A positive correlation was found between the levels of plasma AVP and blood pressure (r = 0.3398, P < 0.01). (5) The concentrations of plasma AVP in hypertensive subjects with ventricular hypertrophy were higher than that in hypertensive subjects with out ventricular hypertrophy (P < 0.05). (6) The concentrations of plasma AVP in hypertensive subjects with heart failure were significantly higher than that in hypertensive subjects with out heart failure (P < 0.001). The results suggest that AVP has a role in the pathogenesis of hypertension, hypertension complicated with ventricular hypertrophy and hypertension complicated with heart failure. The levels of plasma AVP may be viewed as an index of the patient's condition in hypertensive subjects.
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PMID:[The changes in plasma arginine-vasopressin in patients with essential hypertension and the correlation with patient's condition]. 824 27

A genetic model of essential hypertension in the dog was studied to describe the phenotypic expression of the arterial pressure, as well as to determine the relationship between mean arterial blood pressure (MAP), hormone, and renal excretory responses to four different levels of sodium intake (5, 40, 120, 240 mEq/day) delivered intravenously and isotonically. This model was developed at the University of Pennsylvania (U/Penn) and termed Pennsylvania hypertensive dogs (PHD). The MAP was recorded beat-by-beat, 24 h/day, in 16 dogs. Water and sodium balances were determined daily for 4 days at each level of intake and blood samples were collected on the last day of each salt step for analysis of plasma renin activity (PRA), atrial natriuretic peptide (ANP), aldosterone (ALDO), and vasopressin (AVP). After the study, the dogs were designated as hypertensive (PHD-HT) when the 24-h average MAP was greater than 110 mm Hg and systolic pressure was greater than 160 mm Hg. Dogs that failed to meet both criteria were designated as normotensive genetic controls (PHD-NT). Although sodium was retained during the first day of each increase of salt intake in both groups, a return to balance was observed within the 4 days. There was no apparent change in the slope of the chronic renal function curve in either group of PHD studied, although the PHD-HT exhibit a curve shifted to a higher level of MAP. Plasma hormone levels in both groups of PHD studied responded in a manner similar to normal mongrel dogs with reductions of PRA, ALDO, elevations of ANP, and no change in AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pressure-natriuresis relationship in dogs with inherited essential hypertension. 830 71


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