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)

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system. 351 28

In the past, hemodynamic factors, in congestive heart failure were considered as being of major importance in the production of the major symptoms and signs of the disease: peripheral (increased oxygen extraction, flow redistribution) or central (Starling's law, myocardial contractility). More recently, excessive hormonal compensation has been felt to be more important such as: The renine-angiotensin-aldosterone axis, Circulating catecholamines, Arginin-vasopressin. These hormones are responsible for water and sodium retention, tachycardia and increase in peripheral resistance. Newer agents such as Captopril are effective in blocking the action of these endocrine factors.
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PMID:[Treatment of congestive heart failure: new concepts]. 352 15

The effects of 4 weeks of captopril treatment were studied in 10 patients with chronic congestive heart failure (CHF). Acute administration of 50 mg of captopril resulted in an increase in cardiac index and significant decreases in arterial pressure, peripheral vascular resistance and pulmonary capillary wedge pressure. Before treatment, all patients had elevated vasopressin levels (17 +/- 4 pg/ml) relative to decreased plasma osmolality (274 +/- 15 mOsm/kg H2O), and these values were not initially affected by captopril administration (22 +/- 7 pg/ml). However, the relation between arginine vasopressin and plasma osmolality was restored to normal by long-term therapy with captopril (50 mg 3 times daily) (3.0 +/- 1.3 pg/ml; 283 +/- 166 mOsm/kg H2O), which also resulted in sustained improvement of cardiac function. Long-term captopril therapy increased plasma renin concentration from already elevated levels (11 +/- 4 to 32 +/- 8 ng AI/ml X hour) and decreased plasma norepinephrine from 1,054 +/- 244 to 488 +/- 101 pg/ml. Thus, nonosmolar stimulation of vasopressin secretion in CHF can be restored to normal by chronic converting enzyme blockade. The acute vasodilator effects of converting enzyme blockade are not mediated by a reduction of possible vasoconstrictor effects of vasopressin.
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PMID:Vasopressin, renin and norepinephrine levels before and after captopril administration in patients with congestive heart failure due to idiopathic dilated cardiomyopathy. 352 57

Vasopressin's role as a vasoconstrictor in chronic heart failure, was examined in rabbits with adriamycin cardiomyopathic congestive heart failure. Chronic adriamycin treatment resulted in a decrease in cardiac output (829 +/- 38-610 +/- 36 ml/min, P less than 0.005) and blood pressure (83 +/- 2-76 +/- 3 mmHg, P less than 0.01), and an increase in peripheral resistance (8,377 +/- 381-10,170 +/- 657 dyn-s-cm-5, P less than 0.05). Plasma renin activity (4.7 +/- 0.6-10.9 +/- 2.8 ng angiotensin I/ml X h) and norepinephrine (0.7 +/- 0.1-1.3 +/- 0.2 pmol/ml, P less than 0.05) increased while plasma vasopressin levels did not change. Vasopressin infusion, however, produced significantly greater increases in peripheral resistance in animals with heart failure than in controls. Moreover, a specific vasopressin vascular antagonist reduced blood pressure (7 +/- 3%) and peripheral resistance (14 +/- 4%) and increased cardiac output (10 +/- 3%) in animals with heart failure but had no cardiovascular effects in normal rabbits. These results suggest that vascular sensitivity to vasopressin is increased in heart failure, and that it contributes significantly to the increased afterload in heart failure despite normal plasma levels. In this model of severe, chronic heart failure the sympathetic, renin-angiotensin, and vasopressin systems all appear to be activated.
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PMID:Vasoconstrictor role for vasopressin in experimental heart failure in the rabbit. 352 20

Two groups of patients with congestive heart failure were studied, one with elevated (Group I) and another (Group II) with suppressed plasma concentrations of vasopressin. The mean plasma arginine vasopressin (AVP) concentration in the 17 patients in group I was 3.1 +/- 0.4 pg/mliter whereas the eight patients in group II had plasma concentration less than 0.5 pg/mliter. Platelet AVP concentrations were also higher in the Group I than Group II patients (7.8 +/- 1.5 vs. 2.2 +/- 0.7 pg/mliter, P less than 0.001). Plasma effective osmolality (262 vs. 268 mOsm/kg H2O, P less than 0.05) and plasma sodium concentration (134 vs. 137 mEq/liter, P less than 0.05) were lower in Group I. The Group I patients had a lower cardiac index (CI, 1.9 vs. 2.5 liter/min/m2, P less than 0.05) and higher pulmonary capillary wedge pressure (PCWP, 30 vs. 22 mm Hg, P less than 0.02), plasma renin activity (4.4 vs. 2.0 ng/mliter/hr, P less than 0.01), and plasma aldosterone (74 vs. 10 ng/dliter, P less than 0.001) than the Group II patients. The Group I patients also excreted a smaller percentage of a 15 mliter/kg waterload (31 vs. 57%, P less than 0.005). Group I patients then were treated with agents to decrease cardiac afterload, either captopril or prazosin. CI increased (1.9 to 2.1 liter/min/m2, P less than 0.001) and PCWP decreased (30 to 27 mm Hg, P less than 0.001). This improved cardiac performance was associated with enhanced water excretion (31 vs. 52%, P less than 0.001) and decreased minimal urinary osmolality (375 vs. 208 mOsm/kg H2O, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of plasma and platelet vasopressin by cardiac function in patients with heart failure. 352 12

Neurohumoral factors were assessed in 14 subjects with chronic, stable New York Heart Association functional class II or III congestive heart failure and nine comparably aged normal subjects at rest and during moderate (50 W) and strenuous (100 W) upright exercise. Heart failure was associated with elevated plasma renin activity and plasma antidiuretic hormone (ADH) concentrations at rest. However, plasma renin activity almost doubled (from 4.7 +/- 0.6 to 8.4 +/- 1.1 ng/ml per hour) during strenuous exercise in subjects with heart failure, and changed only minimally in normal control subjects. Plasma ADH concentration did not change during exercise in the presence of heart failure, but rose in normal subjects during strenuous exercise to levels comparable to those of subjects with heart failure. Similar plasma osmolality values were present in both groups. Circulating norepinephrine concentrations were insignificantly elevated by heart failure both at rest and during exercise, and plasma epinephrine concentrations were similar. These findings suggest independent neurohumoral activation during exercise in the presence of congestive heart failure, with predominant activation of the renin-angiotensin-aldosterone axis.
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PMID:Neurohumoral activation during exercise in congestive heart failure. 353 88

Congestive heart failure is characterized by peripheral circulatory abnormalities including arterial and venous vasoconstriction and redistribution of regional blood flow. These peripheral factors are consecutive to a neurohumoral activation of sympathetic, renin-angiotensin-aldosterone and arginine-vasopressin systems. Clinical consequences of these neurohumoral changes are: excessive increase of aortic impedance and myocardial work, salt and water retention a processus which is angiotensin II-dependent, and eventually, hyponatremia. A growing body of evidences suggests that pharmacological blockade of this neurohumoral activation improves clinical and hemodynamic status in patients with congestive heart failure.
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PMID:[Neurohormonal factors in congestive heart failure]. 355 7

The incidence of congestive heart failure (CHF) in the elderly increases with age as 80% of patients hospitalised with CHF are older than 60 years of age. In this age group CHF may result from several factors such as coronary artery disease, hypertension, valvular disease or intrinsic myocardiopathies. Important alterations of renal physiology have been observed in this condition: decreases in renal plasma flow and glomerular filtration rate, and increases in renal venous pressure. Natriuretic hormone inhibition occurs and renin-angiotensin-aldosterone system activation and antidiuretic hormone secretion increase, resulting in positive water and sodium balances that contribute to the manifestations of congestive heart failure. The treatment of CHF in the elderly is similar to that in younger patients; the difference in management is determined by the severity of the disease and the side effects of the drugs used. Diuretics increase water and sodium elimination by the kidney and increase the systolic volume of the left ventricle, probably by the reduction of preload and afterload. Diuretic therapy must be pursued carefully in patients receiving digitalis, especially in those elderly individuals who may be on restricted diets: the most common adverse effects of diuretics in this age group are hypovolaemia, hyponatraemia, hypokalaemia and hypomagnesaemia.
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PMID:Diuretic therapy in congestive heart failure for the elderly patient. 373 94

The pathophysiological role of an increase in circulating vasopressin in sustaining global and regional vasoconstriction in patients with congestive heart failure has not been established, particularly in patients with hyponatraemia. To assess this further, 20 patients with congestive heart failure refractory to digoxin and diuretics were studied before and 60 minutes after the intravenous injection (5 micrograms/kg) of the vascular antagonist of vasopressin [1(beta-mercapto-beta,beta-cyclopentamethylene-propionic acid), 2-(0-methyl) tyrosine] arginine vasopressin. Ten patients were hyponatraemic (plasma sodium less than 135 mmol/l) and 10 were normonatraemic. In both groups of patients the vascular vasopressin antagonist did not alter systemic or pulmonary artery pressures, right atrial pressure, pulmonary capillary wedge pressure, cardiac index, or vascular resistances. Furthermore, there was no change in skin and hepatic blood flow in either group after the injection of the vascular antagonist. Only one patient in the hyponatraemic group showed considerable haemodynamic improvement. He had severe congestive heart failure and a high concentration of plasma vasopressin (51 pmol/l). Plasma renin activity, vasopressin, or catecholamine concentrations were not significantly changed in response to the administration of the vasopressin antagonist in either the hyponatraemic or the normonatraemic groups. Patients with hyponatraemia, however, had higher baseline plasma catecholamine concentrations, heart rate, pulmonary pressure and resistance, and lower hepatic blood flow than patients without hyponatraemia. Plasma vasopressin and plasma renin activity were slightly, though not significantly, higher in the hyponatraemic group. Thus the role of vasopressin in sustaining regional or global vasoconstriction seems limited in patients with congestive heart failure whether or not concomitant hyponatraemia is present. Vasopressin significantly increases the vascular tone only in rare patients with severe congestive heart failure and considerably increased vasopressin concentrations. Patients with hyponatraemia do, however, have raised baseline catecholamine concentrations, heart rate, pulmonary arterial pressure and resistance, and decreased hepatic blood flow.
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PMID:Hormonal, global, and regional haemodynamic responses to a vascular antagonist of vasopressin in patients with congestive heart failure with and without hyponatraemia. 379 Mar 79

To assess the role of vasopressin (AVP) in congestive heart failure (CHF), we investigated 10 patients with CHF refractory to conventional treatment, before and 60 minutes after intravenous administration of 5 micrograms/kg of d(CH2)5Tyr(Me)AVP, a specific antagonist of AVP at the vascular receptor level. Heart rate, systemic arterial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac index by thermodilution, and cutaneous blood flow by laser-Doppler technique were measured. In 9 patients there was no significant hemodynamic and cutaneous blood flow response to the AVP antagonist. Plasma AVP was 2.3 +/- 0.8 pg/ml and plasma osmolality 284 +/- 14 mosm/kg H2O. The tenth patient had the most severe CHF. His plasma AVP was 55 pg/ml and plasma osmolality 290 mosm/kg. He responded to the AVP antagonist with a marked decrease in systemic arterial pressure from 115/61 to 79/41 mm Hg, in pulmonary arterial pressure from 58/31 to 33/13 mm Hg and in pulmonary capillary wedge pressure from 28 to 15 mm Hg. Simultaneously cardiac index increased from 1.1 to 2.21 X min-1 X m-2 and cutaneous blood flow rose 5-fold. Thus, most patients with CHF have only moderately elevated plasma AVP and its role in determining peripheral vascular resistance appears to be limited. AVP may become important in rare patients presenting with marked hemodynamic instability and very high plasma AVP.
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PMID:[Hemodynamic effects of an inhibitor of the vascular effects of vasopressin in patients with congestive heart failure]. 384 12


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