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)

The hemodynamic and hormonal changes produced by adriamycin-induced cardiomyopathic congestive heart failure in rabbits were studied. Adriamycin cardiomyopathy in rabbits led to ventricular dilatation, pleural and pericardial effusions, hepatic congestion, and ascites. These pathological changes were associated with the maintenance of a normal blood pressure but a lowered cardiac output and increased total peripheral resistance. Plasma renin activity and plasma norepinephrine were increased twofold in rabbits with congestive cardiac failure. However, plasma vasopressin and osmolality were normal, whereas an increased vascular sensitivity to the infusion of exogenous vasopressin was demonstrated. Despite the normal levels of plasma vasopressin, administration of a specific vascular vasopressin antagonist led to a fall in blood pressure, a significant increase in cardiac output, and a decrease in total peripheral resistance. No such hemodynamic changes occurred on infusing normal rabbits with the vascular vasopressin antagonist, nor did any significant hemodynamic changes occur on injecting vehicle in rabbits with heart failure. These results suggest that in adriamycin-induced cardiomyopathic heart failure in rabbits, there is activation of the renin-angiotensin system and the sympathetic nervous system together with an increased sensitivity to vasopressin. These three hormonal systems help to maintain blood pressure by increasing total peripheral resistance in this experimental model of heart failure.
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PMID:Role of vasopressin in experimental congestive cardiac failure. 243 82

We report the effects of intravenous infusion of the atrial natriuretic peptide analogue, met-ANP-26 (2 micrograms/min for 2 to 4 hours), in four patients with cardiomyopathy and severe congestive cardiac failure who had not received any previous cardiac therapy. The average cardiac index before infusion was 1.8 L/min/m2. Severe sodium and water retention was confirmed by high levels of total body water and extracellular liquid, whereas renal blood flow and glomerular filtration rate were reduced. Plasma concentration of ANP, norepinephrine, cortisol, and growth hormone were significantly increased before infusion. The infusion had no significant hemodynamic effect. After 2 hours urine volume had increased significantly from 51 to 76 ml/hr, urinary concentration of sodium from 72 to 90 mmol/L, and sodium excretion from 4.5 to 8.2 mmol/hr. The infusion was accompanied by a significant increase in plasma ir-ANP from 193 to 980 pg/ml. There were no significant effects on the plasma concentrations of norepinephrine, epinephrine, aldosterone, vasopressin, cortisol, growth hormone, or prolactin and no significant change in plasma renin activity. After 2 hours of infusion one patient had a severe sinus tachycardia and another had a sinus bradycardia. Both arrhythmias disappeared without harmful effects soon after the infusion was stopped.
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PMID:Hemodynamic, hormonal, and renal effects of atrial natriuretic peptide in untreated congestive cardiac failure. 252 77

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

The role of atrial natriuretic peptide in the pathophysiology of heart failure is unknown. The aim of the study were changes of atrial natriuretic peptide, hemodynamic, renal and hormonal parameters during the development of cardiac failure in an animal model of congestive heart failure in the conscious dog due to rapid right ventricular pacing and in rats with chronic left ventricular failure due to a left ventricular infarction. The effects of intravenous administration of atrial natriuretic peptide were studied in patients with severe congestive heart failure, dogs with experimental cardiomyopathy and conscious rats with acute right ventricular failure due to repeated pulmonary emboli. The results suggest an important role of atrial natriuretic peptide in the early phase of heart failure as a counterregulating system concerning vasoconstrictory and volume retaining mechanisms like the renin-angiotensin-aldosterone system, the sympathetic nerve activity and vasopressin. In chronic heart failure the renal effects of atrial natriuretic peptide are attenuated. Pharmacological doses have beneficial effects on ventricular function by reducing pre- and afterload. The reduction in effectiveness of atrial natriuretic peptide in congestive heart failure may be due to a down-regulation of specific receptors, or caused by hemodynamic renal changes preventing the action of the hormone on the kidney in heart failure or may be due to an activation of counterregulating systems overridding the effects of atrial natriuretic peptide.
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PMID:[Atrial natriuretic peptide in cardiac insufficiency]. 296 47

The systemic effects of local anesthetic drugs, especially bupivacaine, on myocardial conduction and the increase of cardiotoxicity by hypoxemia, acidosis, and hyperkalemia has been proven in numerous animal experiments. In our department, supraclavicular brachial block with bupivacaine is the method of choice for patients with chronic renal failure requiring operations of the upper limb. The question may be raised whether or not these patients with their concomitant disease--electrolyte and acid-base imbalances, uremic cardiomyopathy--are especially endangered by the use of this drug. Supraclavicular brachial blockade (3 mg/kg bupivacaine 0.5% + 0.1 IU vasopressin/ml) was performed in 10 patients with chronic renal failure requiring hemodialysis. The control group consisted of 10 healthy patients who were admitted for minor hand surgery. Preoperative blood samples were taken for measurements of blood urea nitrogen, serum creatinine, serum electrolytes, and arterial blood gas analysis. Long-term ECG monitoring begun 20 min before injection of the block and continued over a total of 200 min. Serum concentrations of bupivacaine were determined at 10, 20, 30, 60, 120, and 180 min after injection. Comparing the two groups, no severe changes in electrolytes or acid-base status could be found despite some statistical significances. Even though bupivacaine serum concentrations proved to be 3 times higher in the study group than in the control group, no changes in cardiac conduction could be registered. We conclude that bupivacaine is as safe in dialyzed patients with chronic renal failure with regard to possible changes in circulatory parameters and myocardial conduction as in healthy patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative study of circulatory and ECG-changes after supraclavicular plexus block with bupivacaine-HCl 0.5 per cent in patients with chronic kidney failure]. 365 36

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)
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PMID:Adriamycin cardiomyopathy in the rabbit: an animal model of low output cardiac failure with activation of vasoconstrictor mechanisms. 401 15

Hamsters of the BIO 14.6 strain characteristically develop cardiomyopathy as they age, and hamsters of this strain have overt signs of heart failure by 11 months of age. Plasma levels of the posterior pituitary hormone arginine-vasopressin (AVP) were found to be elevated (approximately 2-fold) in 11 month old BIO 14.6 hamsters, compared to age-matched hamsters of a control strain. AVP appeared inappropriately elevated in these animals, since they were neither hyperosmotic nor markedly hypotensive. The elevated levels of AVP observed in these animals appears to contribute to vasomotor tone, since intravenous administration of a specific antagonist of the vasoconstrictor action of AVP [d(CH2)5Ome(TYR)AVP] elicited a fall in arterial pressure (9 +/- 2 mm Hg, n = 6, p less than 0.05). The AVP antagonist had no effect on arterial pressure in hamsters of a control strain, and vehicle administration had no effect on arterial pressure in either strain. These data indicate that inappropriately elevated levels of AVP contribute to the cardiovascular state of myopathic hamsters. Since elevated plasma AVP has been noted in human congestive heart failure, these results suggest that AVP may contribute to the cardiovascular status during congestive heart failure.
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PMID:Elevated plasma vasopressin in cardiomyopathic hamsters. 406 3

Hyponatremia has been recognized as a complication in adults with acquired immunodeficiency syndrome (AIDS). We did a retrospective study evaluating the medical records of 86 children (age 4 months to 21 years) with human immunodeficiency virus (HIV-1) infection to determine the frequency and clinical associations of hyponatremia. Twenty-two children (26%) developed hyponatremia (serum sodium < 135 mEq/L; range 104 to 134 mEq/L; mean 130 mEq/L). Fourteen were male; 18 of the 22 patients were black and 4 were white. At the time of hyponatremia, the children frequently had comorbid associations, including 8 (35%) with AIDS encephalopathy; 3 (14%) with cardiomyopathy; 3 (14%) using diuretics; 1 (5%) using pentamidine; 3 (14%) with bacterial pneumonia; 2 (9%) requiring gastric lavage feedings; 2 (9%) with tuberculosis meningitis; 2 (9%) with gastroenteritis; 1 (5%) with infection caused by Mycobacterium avium-intracellulare; 1 (5%) each with brain tumor and tumor metastasis to brain. The cause of hyponatremia was attributed to syndrome of inappropriate antidiuretic hormone in 8 children; poor sodium intake and/or excessive diarrheal losses in 5; and the use of diuretics in 3 patients. Mild hyponatremia with no identifiable cause was found in 5 patients.
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PMID:Hyponatremia in pediatric patients with HIV-1 infection. 748 60

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.
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PMID:Interaction between the actions of taurine and angiotensin II. 1094 14

Patients with cirrhosis and portal hypertension exhibit characteristic hemodynamic changes with hyperkinetic systemic circulation, abnormal distribution of blood volume and neurohumoral dysregulation. Their plasma and noncentral blood volumes are increased. Splanchnic vasodilation is of pathogenic significance to the low systemic vascular resistance and abnormal volume distribution of blood, which are important elements in the development of the concomitant cardiac dysfunction, recently termed 'cirrhotic cardiomyopathy'. Systolic and diastolic functions are impaired with direct relation to the degree of liver dysfunction. Significant pathophysiological mechanisms are reduced beta-adrenergic receptor signal transduction, defective cardiac excitation-contraction coupling and conductance abnormalities. Vasodilators such as nitric oxide and calcitonin gene-related peptide are among the candidates in vasodilation and increased arterial compliance. Reflex-induced, enhanced sympathetic nervous system activity, activation of the renin-angiotensin aldosterone system, and elevated circulation vasopressin and endothelin-1 are implicated in hemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the hemodynamic and neurohumoral abnormalities in cirrhosis are part of a general cardiovascular dysfunction, influencing the course of the disease with the reduction of organ function, with sodium and water retention as the outcome. These aspects are relevant to therapy.
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PMID:Splanchnic and systemic hemodynamic derangement in decompensated cirrhosis. 1124 Mar 79


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