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)

Baseline serum prolactin (PRL) was found to be similar in 35 men with untreated essential hypertension (149 +/- 2/98 +/- 1 mmHg; means +/- s.e.) and 44 healthy normotensive men (126 +/- 1/80 +/- 1 mmHg), all 40 years old. A correlation between baseline PRL and aldosterone was found in the normotensive (r = 0.534, P less than 0.001), but not in the hypertensive group (r = -0.011, NS). Ten subjects from each group received intravenous metoclopramide, a competitive dopamine antagonist, while another 12 normotensive subjects were given saline only, and the effect on PRL, vasopressin (AVP) and catecholamines was followed. An exaggerated PRL response to metoclopramide was observed in the hypertensive group compared with the normotensive (P less than 0.05), and the mean normotensive peak value never exceeded the hypertensive. Plasma noradrenaline increased significantly compared with baseline (P less than 0.05) and the control group (P less than 0.001), concomitant with increased heart rate (P less than 0.05), after the administration of metoclopramide both in the hypertensive and normotensive group. After intravenous injection of metoclopramide, forearm blood flow increased significantly by 50% in the hypertensive (P less than 0.001), and 80% in the normotensive group (P less than 0.001) compared with the control group. Mean blood pressure remained unchanged as did plasma AVP, dopamine and adrenaline. The present study indicates an altered central dopaminergic activity in essential hypertension. Even at rest, endogenous dopamine exerts a modulating effect on noradrenaline release in both hypertensive and normotensive men.
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PMID:Decreased central dopaminergic activity in essential hypertension. 361 68

The functional and morphologic characteristics of isolated subcutaneous resistance vessels (about 170 micron i.d.) from 15 untreated subjects with essential hypertension and 15 matched controls were examined. The vessels from the hypertensives had a 29% increase in the media-thickness-to-lumen-diameter ratio. The maximal force development to noradrenaline (NA) expressed as active pressure (an estimate of the pressure the vessels could have contracted against in vivo) was 30% higher in vessels from the hypertensives, while active media stress (force per square unit of smooth muscle) and sensitivity to NA was not significantly different. Increased active pressure, as well as unaltered active media stress and sensitivity, was seen for vasopressin, serotonin, angiotensin II, and K+. There was, however, an enhanced leftward shift of the NA sensitivity with cocaine (an inhibitor of the neuronal amine pump) in vessels from the hypertensives [pD2(+cocaine) and pD2(-cocaine) were 0.185 +/- 0.53) and 0.040 +/- 0.044, hypertensives and normotensives, respectively, p less than 0.05] suggesting an abnormality of presynaptic function in essential hypertension. Furthermore, the calcium sensitivity was depressed (pD2 was 4.197 +/- 0.050 and 4.381 +/- 0.068, hypertensives and normotensives, respectively, p less than 0.05), and the rate of relaxation was faster (p less than 0.05) in vessels from hypertensives, suggesting that excitation-contraction coupling might be depressed. The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.
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PMID:Evidence for increased media thickness, increased neuronal amine uptake, and depressed excitation--contraction coupling in isolated resistance vessels from essential hypertensives. 362 84

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.
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PMID:Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia. 385

To assess the relationship between pressor and depressor factors in essential hypertension, the urinary excretion rates of prostaglandins E2 and F2 alpha, kallikrein, vasopressin and aldosterone were compared between 53 untreated hypertensive patients and 53 age- and sex-matched normotensive controls. Mean basal levels of plasma renin activity and of urinary prostaglandins, vasopressin and aldosterone were similar in both groups, but urinary kallikrein was significantly lower in the hypertensive patients. A weak relationship was found in the hypertensives between diastolic blood pressure, and vasopressin or aldosterone, and between vasopressin and prostaglandin E2, and in the normotensives between vasopressin and prostaglandin F2 alpha. In conclusion, these results do not provide evidence for an important imbalance between pressor and depressor factors in essential hypertension, as reflected by the urinary excretion of the major humoral factors and hormones involved in the regulation of blood pressure.
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PMID:Urinary excretion of renal prostaglandins, kallikrein, vasopressin and aldosterone in essential hypertension. 386 81

The vasoconstrictor and vasopressor actions of vasopressin have been revealed in recent research through the use of highly specific and sensitive radioimmunoassays, employment of peptide antagonists, and comparison with an animal model which has hereditary absence of this hormone, the Brattleboro rat. Factors now known to modify the pressor effect of vasopressin are the baroreflexes, local vascular prostaglandin production, and a specific interaction with angiotensin II. In experimental models the volume retaining, but not the vasoconstrictor effect of vasopressin is necessary for mineralocorticoid-salt hypertension. Vasopressin contributes directly to the increase in arterial pressure of glycerol induced acute renal failure. In nephrectomized rats, plasma vasopressin is elevated and contributes directly to maintenance of pressure. Vasopressin antagonism may reduce arterial pressure in Goldblatt 1 and 2 kidney hypertension and in one genetic model, spontaneously hypertensive rat (SHR), but the peptide is not necessary for hypertension in these models. Plasma vasopressin is reduced in primary aldosteronism, but may be elevated in malignant hypertension. In essential hypertension, there is considerable disagreement among various studies in which plasma vasopressin, urine vasopressin excretion, platelet associated vasopressin, or vasopressin-neurophysin were measured as to whether there is evidence for increased secretion of vasopressin. Only preliminary studies of vasopressin antagonism in clinical hypertension have been reported. At present, there is no conclusive evidence that elevated vasopressin secretion occurs or is necessary for any form of clinical hypertension.
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PMID:The role of vasopressin in experimental and clinical hypertension. 388 2

The relationships between arterial pressure (BP) and plasma vasopressin levels, plasma renin activity, and other variables were determined in 96 untreated essential hypertensive men (146/100 mm Hg) and women (153/102 mm Hg) whose average age was 44 years, 80 normal men and women (121/79 mm Hg; mean age, 47 +/- 2 years), and 40 subjects defined as borderline hypertensive. An analysis of variance indicated significant sex differences in the population. Levels of plasma vasopressin were significantly elevated in hypertensive men, with 26% (high plasma vasopressin hypertensive) exhibiting levels greater than 2 SD of the normal mean, and multivariate regression analysis indicated a significant positive correlation between plasma vasopressin levels and systolic and diastolic blood pressure. Hypertensive men had a larger daily urine volume than normal men. Diastolic pressure and heart rate were significantly elevated in a subgroup of 12 weight-matched and age-matched hypertensive men in the high plasma vasopressin group compared with levels in normal plasma vasopressin hypertensive men. Hypertensive women had lower plasma renin activity than normal women, and multivariate analysis indicated a significant negative correlation between plasma renin activity and systolic and diastolic blood pressure. Other significant abnormalities in both sexes were noted: hypertensive men and women weighed more and excreted more sodium per day, and both had higher heart rates. With a discriminant analysis of 18 variables in male subjects, plasma vasopressin levels, urinary sodium excretion, and heart rate correctly classified 71% of normal and hypertensive subjects. In women, plasma renin activity, urinary sodium excretion, and heart rate correctly classified 77% of normal and hypertensive subjects. Despite the inability to ascertain causal relationships, the ability of the three variables in combination to correctly classify normal and hypertensive subjects indicates that these combined variables are reproducibly altered in persons with essential hypertension.
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PMID:Sex differences in the endocrine predictors of essential hypertension. Vasopressin versus renin. 388 37

The antihypertensive effect of clonidine hydrochloride delivered at a constant rate for seven days by transdermal disks was evaluated in seven patients with essential hypertension. Blood pressure values measured at the physician's office were not significantly decreased by one month of treatment with one (n = 2) or two (n = 5) once-weekly applied clonidine transdermal disks. In contrast, blood pressure values recorded during patients' customary daily activities by means of a portable blood pressure recorder were considerably reduced, from 159/97 +/- 2/2 to 136/76 +/- 7/5 mm Hg. Plasma drug concentration at the end of the fourth week averaged 1.22 +/- 0.24 ng/mL. Plasma renin, vasopressin, and epinephrine levels were not modified by clonidine, whereas plasma norepinephrine level was significantly reduced. Local skin erythema developed in three patients and dry mouth in six. These findings suggest that clonidine transdermal disks lower blood pressure in hypertensive patients, but produce local skin lesions and general side effects.
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PMID:Transdermal clonidine therapy in hypertensive patients. Effects on office and ambulatory recorded blood pressure values. 396 74

Intrinsic vascular responsiveness to norepinephrine, transmural electrical stimulation, 5-hydroxy-tryptamine, and vasopressin was studied in isolated helical cut strips of cystic artery (downstream branch of hepatic artery) from 120 subjects and related to blood pressure. Blood pressure, thickness of the tunica media, and passive elastic properties of arterial strips were each significantly correlated with age. With the exception of blood pressure in the female subjects, it is doubtful that these relationships are of major biologic significance. Nevertheless, in subgroup formation, care was taken to control for age. Hypertension was arbitrarily defined in three different ways as: (a) two diastolic pressure measurements greater than or equal to 90 mm Hg (HT90); (b) two diastolic pressure measurements greater than or equal to 95 mm Hg (HT95); or (c) treatment for hypertension instituted by a physician 6 months to 2 years after arteries were studied (HTQ). In arteries of hypertensive female subjects, responsiveness to norepinephrine (and possibly to 5-hydroxytryptamine) was increased significantly over the first half of the dose-response curve, particularly in the arteries of HT95 and HTQ subjects. Responses to transmural electrical stimulation and vasopressin were not consistently different. Such differences were not seen in arteries of male subjects where, if anything, responsiveness to norepinephrine (but not 5-hydroxytryptamine) was decreased. The present observations were made in the absence of any substantive difference in arterial dimensions (e.g., cross-section area) or in the maximal response to norepinephrine. The data support the notion that, at least for female subjects, alteration in intrinsic vascular responsiveness may play a role in the pathogenesis of human essential hypertension.
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PMID:Relationship of blood pressure to the responsiveness of an isolated human artery to selected agonists and to electrical stimulation. 608 64

In a double-blind versus placebo preliminary study conducted in seven mildly hypertensive patients, the 10-mg capsule form of nifedipine was able to reduce significantly systolic and diastolic blood pressure (-14%) for 3 h. In a single-dose, cross-over study, captopril (1 mg/kg) and nifedipine (20 mg) significantly reduced blood pressure in 12 patients with moderate essential hypertension, but 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). Nifedipine did not significantly alter the renin angiotensin aldosterone system in supine and upright positions, and the blood pressure drop it induced was not related to the initial level of activation of that system. Associated with the stimulation of the sympathetic nervous system, an increased release of vasopressin was noted during nifedipine administration. Finally, nifedipine, a calcium antagonist, was a potent antihypertensive drug through its vasodilating properties. It provoked specific hormonal alterations, i.e., stimulation of catecholamines and vasopressin release, whereas the renin angiotensin aldosterone system was not significantly altered.
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PMID:Acute antihypertensive and hormonal effects of a calcium antagonist in essential hypertension. 618 64

The corticotropic function of the adenohypophysis was investigated in patients with essential hypertension considering the stage of the disease and development of crisis. There was found functional activation of the system under study at the labile stage of essential hypertension without crisis as well as in patients with crisis at labile and stable stages of the disease. Unidirectional shifts were observed in the function of the vasopressor part of the hypothalamus-neurohypophyseal system.
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PMID:[Adrenocorticotropic hormone in hypertension]. 628 83


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