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)

Study I: A retrospective survey of the data base on serum electrolyte measurements in our hospital (approximately 50,000 cases) revealed that the incidence of hyponatremia increased with age. Its major cause in the elderly hospital inpatients with cardiovascular disease was congestive heart failure, frequently accompanied by renal dysfunction and the use of diuretics. Another interesting finding from this analysis was that the use of potassium sparing diuretics were often associated with hyperkalemia in elderly patients whose renal functions were apparently normal based on the serum creatinine level. Study II: The resting hemodynamics and the plasma levels of various hormones related to water and electrolyte metabolism were compared between normal elderly and young subjects. The resting hemodynamic parameters, including cardiac index and blood pressure, did not differ between the two normal groups. Plasma atrial natriuretic peptide and norepinephrine levels were significantly higher in the elderly, while plasma renin activity and aldosterone levels were significantly decreased. No differences were observed in antidiuretic hormone levels. The same parameters were then compared between normal and hypertensive elderly subjects. Elderly hypertensives had lower cardiac index and higher peripheral resistance than normal elderly subjects. Plasma norepinephrine level and plasma renin activity were lower, but aldosterone level was not significantly lower in hypertensives than in normotensives. There was no difference in antidiuretic hormone. In the elderly group as a whole, atrial natriuretic peptide correlated positively with blood pressure, and negatively with plasma norepinephrine and renin activity. Multivariate analysis showed that the strongest correlation was that with plasma renin activity. These results suggest that the plasma levels of various hormones related to water and electrolyte metabolism were altered with age and hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Water and electrolyte metabolism in the elderly with cardiovascular disease--hormonal aspects in elderly hypertension]. 279 73

We performed a randomized double-blind placebo controlled cross-over study of enalapril in 16 patients with chronic congestive heart failure, to assess haemodynamic and hormonal effects at rest and on exercise. Acute effects were measured 4 h after enalapril 10 mg, and chronic effects after 6 weeks treatment with enalapril 10-20 mg per day. Exercise tolerance, assessed by the duration of a maximal bicycle ergometer test, was not altered by enalapril. Mean blood pressure was reduced after enalapril, at rest and on exercise, acutely by 7% and 8% respectively, and chronically by 14% and 16%. Systemic vascular resistance was reduced by 16% at rest both acutely (NS) and chronically (p less than 0.05). The resting pulmonary capillary wedge pressure was reduced by 28% with chronic treatment. In the acute study, total body oxygen consumption on exercise was 26% higher after enalapril. Chronically, resting oxygen consumption was reduced by 13% after enalapril, with mixed venous oxygen saturation increasing by 16%. In the acute study enalapril increased plasma renin activity at rest and on exercise by 181% and by 189%, and reduced aldosterone by 49% (NS) and 39% (p less than 0.05), and these effects were sustained after 6 weeks. Enalapril increased antidiuretic hormone concentrations at rest acutely by 73% (NS) and chronically by 34% (p less than 0.05) but not on exercise; the increase in the acute study correlated with plasma enalaprilat levels (r = 0.66, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A randomized cross-over study of enalapril in congestive heart failure: haemodynamic and hormonal effects during rest and exercise. 284 Nov 36

The effects of nitrates on a Ca+2 increase and the content of cyclic nucleotides in human platelets were studied. Nitroglycerin (GTN), isosorbide dinitrate (ISDN) and sodium nitroprusside (NP) were found to inhibit dose-dependently the intracellular Ca+2 increase induced by the platelet activating factor (PAF). The inhibiting effect of NP was at lower concentrations than those of GTN and ISDN. GTN calcium blocking action did not change significantly regardless of vasopressin, serotonin or PAF used as inducers of the intracellular Ca+2 increase. GTN suppressed the PAF provoked Mn+2 entering into the cells. NP and GTN induced increase of the cGMP content correlated with their calcium blocking activity. They did not augment the level of cAMP. Methylene blue (MB), a guanylate cyclase and glutathione reductase inhibitor, decreased the calcium blocking effect of GTN and its influence on the cGMP content but failed to suppress the inhibitory effect of NP. Ascorbic acid increased the calcium blocking effect of NP but did not influence the inhibitory effect of GTN. An increase in Ca+2 content induced by PAF in platelets from patients with chronic congestive heart failure was significantly higher in the group with dilatation cardiomyopathy. The effect of 10 mg of ISDN sublingually on forearm venous tone was higher in patients with initially elevated venous tone. There was a direct statistical correlation between the IC50 of GTN calcium blocking effects in platelets and the elevation of a forearm venous tone reaction from a statistic mean reaction to ISDN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[New approaches to the study of the mechanism of action of nitrates]. 285 8

Plasma concentrations of immunoreactive atrial natriuretic peptide (ANP) were low or undetectable in 8 healthy subjects and 9 control patients without cardiac disease, and raised in 17 patients with congestive heart failure (CHF). Highest concentrations were measured in patients with severe CHF. High plasma ANP levels were also found in 2 patients with paroxysmal supraventricular tachycardia and associated transient polyuria. Infusion of synthetic human alpha-ANP, 110-125 micrograms over 30 min, to 3 healthy males resulted in a 2.3-fold increase in natriuresis and diuresis but had no effect on kaliuresis. Plasma levels of renin activity, aldosterone, and antidiuretic hormone did not change significantly. ANP infusion gave plasma ANP levels of the same magnitude as those found in severe CHF; levels returned to baseline within 15 min of stopping the infusion. Thus ANP appears to be a circulating hormone in man, at least in severe CHF and supraventricular tachycardia.
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PMID:Plasma atrial natriuretic peptide in cardiac disease and during infusion in healthy volunteers. 286 25

By means of specific inhibitors of the renin-angiotensin system (captopril) and of the sympathetic nervous activity (prazosin) in dogs with congestive heart failure, and by using a specific antagonist of the pressor activity of arginine vasopressin in rats with heart failure, we studied the influence of these pressor hormone systems on peripheral vascular resistance and cardiac function. All three humoral vasoconstrictor systems were stimulated in heart failure. The experiments in dogs showed that the renin-angiotensin system plays an important role in the pathogenesis of heart failure by increasing peripheral vascular tone, thus impairing cardiac function, a mechanism which could be nearly completely prevented by converting enzyme inhibition. The increased sympathetic nervous activity was only insignificantly attenuated by the converting enzyme inhibition and its contribution to the increase of peripheral vascular resistance was only small and transient. The rats with heart failure showed no effect on the vasopressin inhibitor on peripheral vascular resistance and cardiac function, despite plasma vasopressin levels which were 4 to 5 times higher than those in control animals. The inappropriately high secretion of vasopressin in relation to a decreased plasma osmolality may have contributed to the formation of edema and to the development of 'dilutional hypoosmolality'.
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PMID:Neurohumoral vasoconstrictor systems in heart failure. 286 48

The renal hemodynamic and neurohumoral determinants of sodium and water excretion abnormalities were studied in 66 patients with severe chronic congestive heart failure. Abnormalities were not closely related to any one variable but were the result of the convergence of a number of determinants. The most important determinants for sodium excretion were activation of the renin-angiotensin system and ventricular function; and the most important for water excretion were plasma vasopressin, plasma norepinephrine, and renal and ventricular functions. In a subgroup of patients, neurohumoral overactivation led to severe sodium and water excretion abnormalities and to increased furosemide requirements. A 17-month follow-up of all 66 patients showed a less favorable clinical course for this subgroup even when compared with hemodynamically matched patients.
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PMID:Sodium and water excretion abnormalities in congestive heart failure. Determinant factors and clinical implications. 287 71

Nisoldipine, a calcium entry blocker, was given to 10 patients with congestive heart failure. During a 2 month follow-up period, 7 of the 10 patients were readmitted with pulmonary edema; daily furosemide doses were increased (128 +/- 87 to 192 +/- 135 mg/day, p less than 0.01), and plasma creatinine increased (1.5 +/- 0.5 to 1.8 +/- 0.6 mg/dl, p less than 0.05) (all values mean +/- SD). Despite this unfavorable clinical course, nisoldipine caused some beneficial chronic (1 month) hemodynamic effects. It decreased systemic vascular resistance (from 1,781 +/- 229 to 1,306 +/- 345 dynes X s X cm-5, p less than 0.01), decreased mean arterial pressure (from 88 +/- 0 to 74 +/- 4 mm Hg, p less than 0.001) and increased stroke volume index (from 27 +/- 6 to 33 +/- 9 ml/min per m2, p less than 0.02). Heart rate, pulmonary capillary wedge pressure and stroke work index did not change. However, nisoldipine's chronic renal and neurohumoral effects were not as favorable. These were assessed during a 5 hour water load (15 ml/kg body weight of 5% dextrose in water) and compared with the effects of a water load before therapy. Nisoldipine did not change creatinine clearance or sodium excretion, but decreased water excretion (from 58 +/- 35 to 46 +/- 40% of water load in 5 hours). Over this 5 hour study, mean plasma vasopressin was also higher with nisoldipine (1.9 +/- 2.3 versus 2.7 +/- 3.2 pg/ml, p less than 0.05), but mean plasma aldosterone was lower (67 +/- 31 to 47 +/- 27 mg/dl, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. 288 Aug 84

A series of neurohumoral systems are activated in congestive heart failure that contribute to the increased vascular resistance and sodium retention that characterize this disorder. Abnormalities in baroreceptor function are intrinsic to the pathophysiology of heart failure and may subserve the vasoconstrictive and volume overloaded state that defines patient morbidity. Blunted baroreceptor responses to high cardiac filling pressures or depressed cardiac function reduce afferent signals that normally inhibit sympathetic efferent activity, vasopressin release, and indirectly, renin secretion. The resulting increase in neurohumoral activity mediates the redistribution of blood flow that occurs in this disorder. Limb blood flow is usually reduced and may be responsible for exercise intolerance. Decreased renal blood flow and altered intrarenal hemodynamics contribute to sodium retention. In addition, renal vasoconstriction and elevated circulating levels of angiotensin II and vasopressin may contribute to hyponatremia by influencing free water intake and excretion. Hence, baroreceptor dysfunction may be a principal mechanism that contributes to neurohumoral activation and subsequent alteration in vascular resistance and sodium and water balance in congestive heart failure. It may not be coincidental that two principal markers of an unfavorable prognosis in patients with heart failure, high plasma norepinephrine levels and hyponatremia, share baroreceptor dysfunction as a common theme.
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PMID:Baroreceptor function in congestive heart failure: effect on neurohumoral activation and regional vascular resistance. 288 66

The effects of human alpha atrial natriuretic factor following bolus injection of increasing doses and during a continuous 30 minute infusion were investigated in 7 patients with severe congestive cardiac failure (NYHA III-IV). The natriuretic factor was measured in plasma before and after the bolus application or infusion. The plasma levels were raised in 6 patients. A significant inverse correlation was observed between the basal levels of the atrial factor and cardiac output. In addition, there was a dose-dependent fall in preload and afterload as well as in the peripheral vascular resistance and there was an improvement in cardiac performance. The alpha atrial natriuretic factor inhibited aldosterone and cortisol secretion and promoted diuresis and the urinary excretion of sodium and potassium. The plasma concentrations of renin, noradrenaline, vasopressin, 6-keto-prostaglandin F1 alpha, the stable metabolite of prostacyclin, and prostaglandin E2 remained unchanged.
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PMID:[The atrial natriuretic factor in severe congestive heart failure. Plasma level, hemodynamic, hormonal and renal effects]. 293 Dec 68

The peak hemodynamic effect and hormonal response of the phosphodiesterase inhibitor enoximone (MDL 17,043) were compared with those of dobutamine in 10 patients with severe congestive heart failure. Both agents significantly (p less than 0.05) increased cardiac index, stroke volume index and heart rate. Enoximone tended to decrease mean systemic arterial and pulmonary artery wedge pressures (0.05 less than p less than 0.1), whereas dobutamine did not. Both agents decreased systemic vascular resistance (p less than 0.05). The increase in heart rate was greater with dobutamine than with enoximone (p less than 0.05). Plasma renin activity increased significantly with dobutamine (from 11.3 +/- 13.5 to 17.8 +/- 15.0 ng/ml/hour, p less than 0.01) and with enoximone (from 13.6 +/- 18.3 to 16.6 +/- 18.8 ng/ml/hour, 0.05 less than p less than 0.1). Dobutamine suppressed plasma norepinephrine level (p less than 0.05) and enoximone did not. Neither agent affected the plasma vasopressin level. These data demonstrate a similar acute hemodynamic and hormonal profile for both enoximone and dobutamine. Further, dobutamine, like other beta agonists, provokes renin secretion and may do so to a greater extent than enoximone.
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PMID:Comparative hemodynamic and hormonal response of enoximone and dobutamine in severe congestive heart failure. 294 27


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