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)

Because neurohumoral responses to cardiopulmonary bypass (CPB) are similar to those seen in shock, CPB might be expected to decrease renal blood flow; yet diuresis is commonly observed during and early after routine cardiac procedures with CPB. To examine this apparent paradox, we studied 15 patients before, during, and after CPB for coronary artery bypass grafting. Plasma levels of atrial natriuretic factor (alpha-ANF), aldosterone, and antidiuretic hormone (ADH) and urinary sodium excretion were measured before anesthesia, after sternotomy but before CPB, at 15 and 30 minutes of CPB, and at 15 and 30 minutes after discontinuation of CPB. alpha-ANF increased only slightly during CPB, and the initial natriuresis during CPB occurred in the presence of a markedly increased ADH level. After CPB ended, urine flow and sodium excretion increased in conjunction with increased alpha-ANF and normal ADH. We conclude that the early natriuresis during CPB occurs in the presence of a high ADH concentration, with no significant increase in plasma alpha-ANF. This may be a paradoxic response to supraphysiologic levels of ADH. The natriuresis after CPB appears to be strongly associated with increased alpha-ANF, present for at least the first 30 minutes after CPB, which could reflect alpha-ANF release resulting from atrial distention during volume loading.
J Thorac Cardiovasc Surg 1989 Nov
PMID:Natriuresis during and early after cardiopulmonary bypass: relationship to atrial natriuretic factor, aldosterone, and antidiuretic hormone. 281 28

To study the antihypertensive effect of orally administered taurine in DOCA salt hypertension, urinary excretion of catecholamines, electrolytes, and arg-vasopressin was measured over four weeks in 20 taurine treated DOCA rats (group 1), 20 taurine untreated DOCA rats (group 2), and seven taurine untreated sham operated rats (group 3). Additional experiments were performed to determine whether or not the pressor and sympathetic responses to hypothalamic stimulation were altered after taurine treatment in DOCA rats. Systolic blood pressure decreased significantly in group 1 after the first week compared with that in group 2, and the differences became progressively more evident thereafter. At the fifth week the mean blood pressure was significantly lower in group 1 than in group 2, as was the heart rate. Although urinary excretion of adrenaline decreased significantly in group 1 at the first and fourth weeks, the difference in urinary excretion of noradrenaline between groups 1 and 2 was not significant. Urinary excretion of adrenaline and noradrenaline in group 3 was significantly lower than that in both hypertensive groups (groups 1 and 2). Urinary sodium excretion increased significantly in group 1 at the first and second week compared with group 2. With graded electrical stimulation of the ventromedial hypothalamus, resulting pressor and sympathetic responses were significantly smaller in group 1 than in group 2. These results suggest that the hypotensive effects of orally administered taurine in DOCA hypertensive rats are caused by suppression of the peripheral sympathetic nervous activity and by the resulting natriuresis.
Cardiovasc Res 1988 May
PMID:Retardation of the development of hypertension in DOCA salt rats by taurine supplement. 319 19

The effects of a continuous iv infusion (osmotic minipumps) of angiotensin II (80 ng . kg-1 . min-1) and isoprenaline (10 ng . kg-1 . min-1) lasting 28 days were studied in six normotensive, conscious dogs. The parameters measured were systolic and diastolic blood pressure, heart rate, levels of angiotensin II, renin activity, aldosterone and antidiuretic hormone in plasma, baroreceptor reflex sensitivity and body weight. The treatment resulted in an approximately sevenfold increase in plasma angiotensin II level from 62.9 +/- 24.5 pg . ml-1 to 455.3 +/- 95.6 pg . ml-1. Systolic and diastolic blood pressure, measured for the first time 2 days after implanting the minipumps, were markedly increased throughout the infusion period (pretreatment value: 123.8 +/- 5.3/68.3 +/- 3.8 mmHg; after 2 days: 159.8 +/- 12.0/100.5 +/- 9.8 mmHg; after 28 days: 159.8 +/- 7.1/98.3 +/- 6.4 mmHg, whereas the heart rate remained unchanged due to the combined effects of angiotensin II and the concomitantly given isoprenaline. A high correlation was found between angiotensin II level in plasma and mean arterial blood pressure (r = 0.846; p less than 0.001). Furthermore, plasma renin activity was markedly suppressed by the treatment, and aldosterone levels rose. Plasma antidiuretic hormone levels were found to be unchanged at the chosen sampling time. A decrease in baroreceptor reflex sensitivity accompanied the development of the hypertensive state. There was also a loss of body weight during the infusion of angiotensin II and isoprenaline. The data provide evidence for the usefulness of the presented experimental protocol as an alternative model of arterial hypertension in chronically instrumented, conscious dogs.
Cardiovasc Res 1985 Nov
PMID:Angiotensin-induced hypertension in conscious dogs: biochemical parameters and baroreceptor reflex. 390 39

Chronic administration of intravenous adriamycin (1 mg . kg-1 twice weekly for 8 weeks) to rabbits resulted in a cardiomyopathy which was similar to that occurring in patients with adriamycin cardiotoxicity. We studied systemic and renal haemodynamics and the activation of vasoconstrictor mechanisms reflected by changes in plasma renin activity (PRA), noradrenaline (NA) and vasopressin (AVP) levels during the development of heart failure in this animal model. By 8 weeks cardiac failure was clearly established. At postmortem all animals had dilated hearts, pleural and pericardial effusions, ascites and hepatic congestion. Heart weights were increased (8.1 +/- 0.7 g in treated animals n = 9 vs 6.0 +/- 0.2 g in controls n = 9 p less than 0.05). Cardiac output (measured by thermodilution) fell at 8 weeks from 799 +/- 61 ml . min-1 to 624 +/- 44 ml . min-1 (n = 6 p less than 0.05) with a parallel fall in mean blood pressure from 85 +/- 2 mmHg to 75 +/- 4 mmHg. Total peripheral resistance rose in four of the six rabbits. Renal blood flow fell from 108 +/- 4 ml . min-1 to 61 +/- 6 ml . min-1 (p less than 0.05) by 8 weeks. Renal vascular resistance increased in all animals. PRA increased from 5.1 +/- 0.5 ng AI . ml-1 . h-1 to 11.6 +/- 2.6 ng AI . ml-1 . h-1 by 4 weeks (p less than 0.05) and remained elevated thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovasc Res 1985 Jun
PMID:Adriamycin cardiomyopathy in the rabbit: an animal model of low output cardiac failure with activation of vasoconstrictor mechanisms. 401 15

We studied the effects of intracoronary vasopressin on the relationship between pressure and flow in the coronary circulation of anaesthetised swine. In addition to measurements at control levels, diastolic pressure-flow relationships were constructed from steady-state points below a coronary pressure of 50 mmHg, where endogenous vasodilatation is strongly stimulated. At baseline pressures, flow fell 28% with maximal vasopressin effect. At all levels of diastolic pressure below 50 mmHg vasopressin also decreased flow, eg, at 30 mmHg flow was depressed by 40%. The slope of the steady-state pressure-flow relationship fell from 1.21 to 0.75 ml.min-1.mmHg-1. The diastolic pressure at which coronary flow ceased rose slightly from 13 to 15 mmHg. Intracoronary adenosine completely prevented vasopressin's effect, and the vasodilator response to adenosine was not attenuated by simultaneous administration of vasopressin. The porcine coronary circulation will constrict in response to vasopressin, not only at normal perfusion pressure, but also at low levels when metabolic vasodilatation is intense. Our study has implications about the therapeutic use of vasopressin, and demonstrates interaction of vasoactive stimuli in the coronary circulation.
Cardiovasc Res 1985 Jul
PMID:Vasopressin-induced coronary constriction at low perfusion pressures. 401 20

Such compounds as clonidine, guanabenz and guanfacine, which stimulate central alpha-adrenoceptors, reduce blood pressure predominantly by reducing sympathetic outflow. Notwithstanding, they also tend to reduce renin secretion, aldosterone, and even vasopressin levels. In some clinical settings, inactivation of the renin-angiotensin system may contribute to their antihypertensive effect. In addition, the absence of sodium retention, which appears to be a special feature of guanabenz, may also have a beneficial effect on blood pressure. In contrast, it is unlikely that a decrease in vasopressin secretion has any major influence on blood pressure.
J Cardiovasc Pharmacol 1984
PMID:Effect of centrally acting antihypertensive drugs on the renin-angiotensin system and vasopressin. 608 28

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.
J Cardiovasc Pharmacol
PMID:Relationship of blood pressure to the responsiveness of an isolated human artery to selected agonists and to electrical stimulation. 608 64

Selective catheterization of the left gastric vein was performed after percutaneous transhepatic portography (PTP) in patients with portal hypertension and esophageal varices. Following the hypothesis that drugs increasing the lower esophageal sphincter (LES) pressure may obstruct the variceal blood flow through the lower esophagus, the effect of different drugs (i.e., intravenous injection of vasopressin, pentagastrin, domperidone and somatostatin and subcutaneous injection of metacholine) on the variceal blood flow was examined. Vasopressin did not change the variceal blood flow; pentagastrin, with its known effect of increasing the LES pressure produced a total interruption of the flow in four of eight patients; domperidone, also known to increase the LES pressure obstructed the variceal blood flow in the only patient examined with this drug; somatostatin has no reported action on the LES but blocked the flow in one of two patients; and metacholine, reported to increase the LES pressure did not produce any change in the flow in the three patients examined. LES pressure was recorded before and during vasopressin infusion in seven patients with portal hypertension and esophageal varices. No reaction on the pressure was found. The patient number in the study is small and the results are nonuniform but still they suggest that drugs increasing the LES tonus might be useful to control variceal blood flow.
Cardiovasc Intervent Radiol 1983
PMID:Pharmacologic influence on esophageal varices: a preliminary report. 613 25

We examined whether the activation of the renin-angiotensin system after intramuscular isoprenaline injection contributes to the simultaneous increase in vasopressin release. Plasma concentrations of vasopressin and angiotensin II were measured in conscious rats using specific radioimmunoassays. Intravenous infusions of angiotensin II caused a dose-dependent increase in vasopressin release. Intravenous infusions of the angiotensin II antagonist saralasin did not diminish the isoprenaline-induced vasopressin release. However, the curve relating the isoprenaline-induced decrease in blood pressure and the concomitant increase in vasopressin levels was shifted to the right and no longer linear in saralasin-treated rats. Nephrectomy diminished the vasopressin release caused by isoprenaline when compared to sham-operation. The correlation between the decrease in blood pressure and the simultaneous vasopressin release was changed in a strikingly similar manner by nephrectomy and by saralasin infusions. It may be concluded that small doses of isoprenaline, which cause only minor decreases in blood pressure, induce vasopressin release via the renin-angiotensin system. However, the contribution of this system to vasopressin release declines as hypotension becomes more severe.
J Cardiovasc Pharmacol
PMID:Role of the renin-angiotensin system in isoprenaline-induced vasopressin release. 616 Mar 30

Arginine vasopressin (AVP), phenylephrine, and noradrenaline were infused intravenously into conscious and unrestrained adult spontaneously hypertensive (SH) rats and the changes in arterial pressure and heart rate were compared to those in Wistar--Kyoto (WKY) rats. The curve expressing the relationship of the increase in arterial pressure to the logarithm of the plasma concentration of AVP for SH rats was shifted to the left of that for WKY rats by a factor of four. In contrast, the dose--response (arterial pressure) curves for phenylephrine and noradrenaline in SH rats were displaced slightly to the right. In WKY rats, heart rate fell more for a given elevation of arterial pressure during infusions of AVP than during infusions of phenylephrine and noradrenaline; in SH rats, the heart rate response were less pronounced than in WKY rats, and the responses to vasopressin, phenylephrine, and noradrenaline were similar. The results are consistent with the interpretation that cardiovascular reflex activity is particularly enhanced during infusions of AVP in normotensive rats. The absence of this phenomenon in SH rats appears to contribute to the enhanced pressor activity of AVP in these rats.
J Cardiovasc Pharmacol
PMID:Pressor responsiveness and cardiovascular reflex activity in spontaneously hypertensive and normotensive rates during vasopressin infusion. 616 62


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