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)

1. A symptomatic diuresis, polyuria, sometimes accompanies paroxysmal tachycardias in man. A study was undertaken in patients with inducible supraventricular tachycardia, irrespective of the symptom of polyuria, to measure simultaneous changes in urine output and plasma hormone levels during the arrhythmia. 2. During 14 episodes of induced tachycardia in 10 patients, there was a significant increase in mean urine flow, which was independent of the state of patient hydration. During a mean tachycardia duration of 30 +/- 3 min, the mean group urine flow increased from 3.2 +/- 2.3 ml/min to 7.6 +/- 3.7 ml/min (P less than 0.001). This was characterized by a consistent increase in free water excretion and a variable increase in sodium excretion. 3. The plasma atrial natriuretic peptide level (five patients) significantly increased from 7.6 +/- 4.6 pg/ml to 34.6 +/- 21.7 pg/ml (P less than 0.02) during the arrhythmia. There was no significant change in the plasma arginine-vasopressin level and a non-significant reduction in plasma renin activity. 4. This study has shown that induced supraventricular tachycardias in man are accompanied by a significant diuresis. The mechanisms responsible remain unknown, but do not appear to involve the plasma arginine-vasopressin level alone.
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PMID:Effect of induced supraventricular tachycardias on changes in urine output and plasma hormone levels in man. 131 Sep 15

Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.
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PMID:Dominance of blood pressure in natriuresis associated with supraventricular tachycardia. 182 64

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.
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PMID:Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia. 183 Apr 49

We investigated the possible role of renal prostaglandin (PG) E2 in natriuresis associated with supraventricular tachycardia (SVT). In five female patients with paroxysmal tachycardia, SVT was artificially induced and then stopped 60 min later. Before, during, and after SVT, plasma levels of arginine vasopressin and atrial natriuretic peptide (ANP) and the urinary excretion of sodium and PGE2 were measured. Polyuria was observed during SVT. However, natriuresis did not occur until immediately after the termination of SVT. During SVT, the plasma levels of arginine vasopressin tended to decrease. When SVT was terminated, the vasopressin levels increased significantly (p less than 0.01). Urinary excretion of PGE2 tended to decrease during SVT and then increased significantly (p less than 0.01) after SVT ended. Urinary excretion of sodium was correlated (r = 0.699, p less than 0.001) with the urinary excretion of PGE2. Plasma ANP increased during SVT, but there was no correlation with urinary sodium excretion. These results suggest that renal PGE2, the biosynthesis of which may be stimulated by a increase in plasma vasopressin, is an important factor contributing to the natriuresis observed after the end of SVT.
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PMID:Possible role of renal prostaglandin E2 in natriuresis associated with supraventricular tachycardia. 214 Nov 77

Elevated plasma levels of atrial natriuretic hormone (ANH) have been found in patients during paroxysmal supraventricular tachycardia (SVT) and other clinical syndromes. However, physiologic effects of this endogenous ANH have not been demonstrated. To determine whether the rise in ANH during SVT is associated with either a natriuresis or kaliuresis, urine sodium and potassium levels were measured in five patients at baseline and during SVT simulated by rapid atrioventricular pacing. Plasma ANH levels increased from 149 +/- 35 pmol/L at baseline to 187 +/- 31 pmol/L (p = 0.007) during SVT. Plasma vasopressin and renin levels were unchanged. Urine sodium levels increased 49% from 1.54 +/- 0.66 mEq/hr at baseline to 2.29 +/- 0.89 mEq/hr (p = 0.044) during SVT, and urine potassium levels increased 22% from 4.14 +/- 0.10 mEq/hr to 5.04 +/- 1.25 mEq/hr (p = 0.018). Urine sodium and potassium levels returned to baseline values 1 hour after pacing. Thus elevated plasma levels of ANH during SVT are associated with both a natriuresis and kaliuresis, which may represent physiologic effects of the endogenously secreted hormone.
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PMID:Natriuresis associated with elevated plasma atrial natriuretic hormone during supraventricular tachycardia. 252 62

The aim of this paper was to study atrial natriuretic factor, plasma renin activity and antidiuretic hormone values during paroxysmal atrial arrhythmias with different ventricular rates before and after pharmacological cardioversion and during chronic atrial flutter-fibrillation. The study was carried out: 1) during acute arrhythmias (atrial flutter-fibrillation or supraventricular tachycardia) and after restoration of normal sinus rhythm in 2 patients without heart disease, in 13 with chronic heart disease and in 6 with acute myocardial infarction; 2) during chronic atrial flutter-fibrillation in 5 patients with chronic ischemic heart disease, without congestive heart failure. Atrial natriuretic factor, aldosterone, plasma renin activity and antidiuretic hormone values were measured by radio-immunoassay. During paroxysmal atrial arrhythmias atrial natriuretic factor levels were higher than normal in all patients, particularly in those with supraventricular tachycardia. Most of the aldosterone measurements were above the normal range. As far as plasma renin activity and antidiuretic hormone values are concerned, levels higher than the normal range were found in the patients with severe hemodynamic impairment. Central venous pressure was above normal in all patients except in the 2 without heart disease, and there was a positive correlation between atrial natriuretic factor and central venous pressure values. After restoration of normal sinus rhythm atrial natriuretic factor values returned to normal except in acute myocardial infarction patients, in 1 chronic ischemic heart disease patient with congestive heart failure and in 3 patients with mitral valve disease. In all patients with chronic atrial flutter-fibrillation and in 5 patients with acute atrial flutter-fibrillation and low rate, above normal atrial natriuretic factor values were found with normal central venous pressure values. Atrial distension due to high central venous pressure values, lack of atrial contraction and rhythmic detension of the atrial stretch receptors, may be considered the major stimuli responsible for atrial natriuretic factor release during acute paroxysmal atrial arrhythmias and atrial flutter-fibrillation with low ventricular rate, respectively.
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PMID:[Atrial natriuretic factor in acute atrial hyperkinetic arrhythmia and chronic atrial fibrillo-flutter]. 252 75

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

A significant diuretic and natriuretic response occurs during paroxysmal supraventricular tachycardia (SVT). Although the diuresis may be secondary to suppression of vasopressin secretion, the etiology of the natriuresis remains unexplained. To determine if atrial natriuretic factor (ANF) could contribute to the polyuric response during SVT, 10 patients were studied: five during spontaneous SVT and five during simulated SVT produced by rapid simultaneous atrial and ventricular pacing. Plasma immunoreactive ANF (IR-ANF) levels measured by radioimmunoassay were obtained at baseline (before and/or 24 to 48 hours after SVT) and after at least 15 minutes of SVT in all patients. During spontaneous and simulated SVT, IR-ANF was significantly elevated (mean +/- SE; 275 +/- 68 pmol/L) compared to baseline (28 +/- 7 pmol/L; p = 0.0036). Similar increases in IR-ANF were noted during both simulated and spontaneous SVT. To determine if this IR-ANF release was related to the increase in heart rate or the rise in right atrial pressure during SVT, IR-ANF levels were also measured in five patients with sinus tachycardia and in six patients with congestive heart failure. IR-ANF was significantly related to right atrial pressure (r = 0.93; p = 0.0009) but not to heart rate (r = 0.46). Thus, IR-ANF is elevated during SVT and may contribute to the natriuretic response. The stimulus to IR-ANF secretion during SVT appears to be related to the rise in right atrial pressure rather than to the increase in heart rate.
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PMID:Plasma levels of immunoreactive atrial natriuretic factor increase during supraventricular tachycardia. 294 10

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.
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PMID:[Plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachycardia and concomitant polyuria (urina spastica)]. 297 Jan 68

Fourteen infants with severe acute bronchiolitis were admitted to the Intensive Care Unit (ICU) of Tunis. This pathology represents 36% of severe bronchopulmonary infections admitted to this ICU. Their age ranged between 2 and 48 weeks (mean: 15 weeks). Eight infants had hypotrophy. Two infants had congenital heart disease and one infant had tracheo-bronchomalacia. Viruses were found in 6/11 patients. Respiratory syncytial virus (RSV) was identified in five patients and an adenovirus in one patient. Five patients had respiratory arrest at ICU admission. Ten infants had evidence of atelectasis on chest X-ray films. Thirteen patients required mechanical ventilation. One infant had inappropriate antidiuretic hormone secretion resulting in convulsions. One infant had supraventricular tachycardia. Both had RSV infection. One patient who had congenital heart disease and RSV infection died. In the other 12 patients receiving mechanical ventilation, the mean duration of ventilation was 9 days (range: 2-30 days). The second patient who had congenital heart disease and RSV infection had severe respiratory sequelae at discharge.
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PMID:[Clinical, therapeutic and developmental aspects of acute bronchiolitis in Tunisia]. 918 23


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