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)

Studies were carried out to determine the contribution of cardiopulmonary receptors to the renal responses to head-out water immersion in the nonhuman primate. Immersion to the suprasternal notch was associated with significant increases in central venous pressure, urine flow, and sodium excretion. The increased sodium excretion was due primarily to a significant increase in the percent of the filtered sodium excreted. Deoxycorticosterone acetate (DOCA) and antiduretic hormone (ADH) had no substantial effects on these responses. The finding of a vasopressin-resistant hyposthenuria is consistent with the natriuresis of immersion being due, at least in part, to a decrease in sodium reabsorption proximal to the diluting segment, possibly the proximal tubule. Bilateral cervical vagotomy had no substantial influence on the renal responses to immersion, demonstrating that cardiopulmonary receptors whose axons traverse the vagus nerves are not necessary for the homeostatic adjustments to central hypervolemia in the primate. Since the renal and cardiovascular responses of the primate to immersion are essentially the same as those seen in man, it is probable that vagal pathways also are not necessary in man. However, it is possible that sympathetic afferents are involved in the natriuresis observed in the primate during immersion.
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PMID:Contribution of vagal pathways to the renal responses to head-out immersion in the nonhuman primate. 41 70

As many as 26 children (20 boys and 6 girls) aged 2.5 to 15.5 years suffering from active nephrotic glomerulonephritis were examined for the intravascular liquid volume and antidiuretic hormone in blood plasma. In accordance with the magnitude of the circulating blood volume, 3 groups of patients were distinguished: group I included patients with hypervolemia, group II with hypovolemia, and group III with normovolemia. In the hypovolemic children, the nephrotic syndrome occurred at an earlier age as compared to the normovolemic children who developed it much later. The patients differed in the content of antidiuretic hormone and total blood protein. In the second group children, secretion of antidiuretic hormone was the highest one, whereas the level of total protein was the least one. A relationship was discovered between the pattern of the nephrotic syndrome and the efficacy of diuretic treatment.
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PMID:[Study of various factors of the pathogenesis of nephrotic edema in children with glomerulonephritis]. 175 20

In the past several years great progress has been made in the understanding of the (patho) physiology of ANP. Because an inhibitor of ANP is not available for human use, there is still discussion about the physiological role of ANP. Nevertheless, from the studies described above the evidence is accumulating that ANP has a role in protecting against fluid overload and hypertension by means of inducing natriuresis, inhibition of the renin-angiotensin-aldosterone system and vasopressin and by vasodilation. The therapeutic potential of modulation of the ANP system seems promising, but must await further research.
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PMID:Atrial natriuretic peptide. 183 64

The association between infections with respiratory syncytial virus and plasma concentrations of antidiuretic hormone was assessed in 48 patients who had been admitted to hospital. The mean (SEM) concentration of antidiuretic hormone was significantly raised in patients with bronchiolitis (9.3 (1.4) ng/l) compared with non-pulmonary respiratory syncytial virus infections that cause apnoea or upper respiratory tract symptoms (6.1 (1.7) ng/l). The highest concentrations of antidiuretic hormone were seen in patients receiving mechanical ventilation (18.0 (6.7) ng/l). There were no differences in mean serum sodium concentrations among the subgroups. Hypertranslucency on chest radiograph or an arterial carbon dioxide tension above 6.67 kPa were associated with a significantly higher concentration of antidiuretic hormone. Increased or normal maintenance fluid intake in children with pulmonary respiratory syncytial virus infections may cause the same symptoms of fluid overload as the syndrome of inappropriate secretion of antidiuretic hormone. Patients with pulmonary respiratory syncytial virus infection, hypertranslucency in chest radiograph, hypercapnia, or mechanical ventilation are at risk for raised concentrations of antidiuretic hormone. Restricted fluid intake and careful monitoring of fluid balance and plasma electrolyte concentrations are therefore necessary in these patients.
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PMID:Excessive secretion of antidiuretic hormone in infections with respiratory syncytial virus. 212 82

About 30% of hemodialyzed patients are suffering from chronic fluid overload despite advice to restrict the oral fluid intake. To investigate the cause of the abnormal drinking behaviour a clinical study was performed in 51 non-diabetic patients with endstage renal disease exhibiting lower interdialysis weight gain (less than 3 kg, n = 17) and increased interdialysis weight gain (greater than 3 kg, n = 34). Blood pressure, body weight self-estimated thirst intensity before and after hemodialysis were analyzed. Biochemical and behavioral variables were measured including hormonal factors of water and sodium metabolism. Significant differences of dry weight, creatinine, urea nitrogen and thirst intensity were found between the two groups. Catecholamines, renin, angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide exhibited a similar pattern in both groups. Atrial natriuretic peptide decreased during hemodialysis in both groups, angiotensin II, however, and norepinephrine showed an exaggerated response to ultrafiltration rate in polydipsic patients. These results suggest that changes in serum osmolality during hemodialysis did not contribute to thirst and drinking behaviour. It seems that postdialytic hypovolaemia together with higher plasma-angiotensin II-levels is responsible for increased oral intake of fluid and excessive weight gain.
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PMID:[Regulation of thirst in end-stage kidney insufficiency]. 214 56

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
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PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80

Extracellular fluid volume (E.C.F.) and plasma volume (P.V.), were measured with sodium sulfate labeled with 35I and 131I human serum albumin, respectively, by the dilution technique in control subjects and in cirrhotic patients without clinical ascites or edema, renal or hepatic failure, gastrointestinal bleeding or diuretics. Results are expressed as mean +/- DS in both ml/m2 and ml/kg. In normal subjects E.C.F. (n = 8) was 7,533 +/- 817 ml/m2 (201.3 +/- 182 ml/kg), P.V. (n = 11) 1,767 +/- 337 ml/m2 (47.2 +/- 9.3 ml/kg), and interstitial fluid (I.S.F.) (n = 7) 5,758 +/- 851 ml/m2 (Table 2). In cirrhotic patients E.C.F. (n = 11) was 10,318 +/- 2,980 ml/m2 (261.7 +/- 76.8 ml/kg), P.V. (n = 12) 2,649 +/- 558 ml/m2 (67.7 +/- 15.6 ml/kg) and I.S.F. (n = 11) 7,866 +/- 2,987 ml/m2 (Table 3). Cirrhotic patients compared with normal subjects have hypervolemia due to a significant E.C.F. and P.V. expansion (p less than 0.02 and less than 0.001 respectively) (Fig. 1). Reasons for E.C.F. and P.V. abnormalities in cirrhotic patients may reflect urinary sodium retention related to portal hipertension which stimulates aldosterone release or enhanced renal tubular sensitivity to the hormone. However, it is also possible that these patients, in the presence of hypoalbuminemia (Table 1), have no clinical edema or ascites due to increased glomerular filtration, suppressed release of vasopressin, increased natriuretic factor, and urinary prostaglandin excretion, in response to the intravascular expansion, all of which increased solute and water delivery to the distal nephron and improved renal water excretion. We conclude that in our clinical experience cirrhotic patients without ascites or edema have hypervolemia because of a disturbance in E.C.F.
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PMID:[Extracellular fluid, plasma and interstitial volume in cirrhotic patients without clinical edema or ascites]. 248 40

Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA), aldosterone (ALD) and vasopressin (VP) were assessed in six heart transplant patients (HTP) and ten healthy subjects under bed rest conditions and 60 and 120 minutes after head-out water immersion (WI). Bed rest had no significant influence on these parameters. WI raised plasma volume (PV) to the same extent in both groups. This increase of PV was accompanied by significant suppression of PRA, ALD and VP and an increase of plasma ANP. In HTP basal plasma ANP was significantly elevated and the ANP response to central hypervolemia reduced. Significantly elevated VP plasma levels were also found in HTP. These endocrine abnormalities in HTP seem to be caused by latent failure of the transplanted heart. No direct correlation was found between plasma ANP and PRA, ALD and VP under basal conditions and after WI in either HTP or normals.
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PMID:Atrial natriuretic peptide secretion in heart transplant patients. 252 31

To examine body fluid regulation over 72 h of recovery from a 24-h endurance race, changes in plasma volume (delta PV) and plasma aldosterone (A), cortisol (CO), antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP) were studied in nine male runners before (C) and after (1-2 h = D0; 24 h = D1; 48 h = D2; 72 h = D3) the race, 24-h urine collections were made 1 week before (C), during the 24-h race/U0), and during the 3 days following the end of the race (U1, U2, and U3). On D0 delta PV decreased (2%). A, CO and ADH increased (380%, 200%, and 133%, respectively, from C values) and ANP decreased (68%). No significant changes were found in sodium, potassium, osmolality in plasma, in 24-h urine volume (UV), and natriuresis (Na+). Urinary potassium excretion (K+) increased (256% from C value). During the 3 days of recovery delta PV rose markedly with a peak on D2 (24%) and remained elevated on D3 (15%). CO, ADH, and ANP returned to baseline on D1 and A on D3. Significant inverse effects were observed on ADH (P less than 0.001) and ANP (P less than 0.01): from C values, ADH decreased (21% and 29%) and ANP increased (41% and 58%) on D2 and D3, respectively. UV and Na+ were depressed on D1 and D2. This study shows that the hormonal responses observed immediately after the 24-h run favored a relative fluid conservation. The hypervolemia that occurred during the 3-day recovery was related to renal responses on D1 and D2 and appeared to be the primary factor in the hormonal responses on D2 and D3.
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PMID:Hormonal, fluid, and electrolyte changes during a 72-h recovery from a 24-h endurance run. 253 21

Fluid overload and dehydration are potentially serious physiologic perturbations. Their effects on the pharmacodynamics of drugs are essentially unknown. This investigation was designed to determine the effects of acute fluid overload or water deprivation on the hypnotic activity of phenobarbital and on the neurotoxicity of theophylline in male Lewis rats. In the first experiment, 5% dextrose in water (D5W) was infused i.v. in an amount equal to 5 or 10% of body weight and phenobarbital was infused immediately thereafter until the onset of loss of righting reflex (LRR). The total infused dose and the serum and cerebrospinal fluid (CSF) concentrations of phenobarbital at that time were significantly lower than in control animals. When phenobarbital was infused about 2.5 hr after D5W, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were normal. When the rats received D5W and an injection of vasopressin, 25 I.U./kg, or vasopressin only, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were significantly lower than in controls despite the 2.5-hr interval between the respective pretreatments and the phenobarbital infusion. Water deprivation for 24 or 48 hr had no significant effect on phenobarbital dose and concentrations at LRR. Intravenous infusion of D5W to 10% of body weight immediately or 2.5 hr before theophylline infusion had no significant effect on the total infused dose and the serum and CSF concentrations of theophylline at onset of maximal seizures. This lack of effect occurred despite appreciable hyponatremia and hypomagnesemia immediately after D5W infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics of drug action in disease states. XXXVII. Effects of acute fluid overload and water deprivation on the hypnotic activity of phenobarbital and the neurotoxicity of theophylline in rats. 260 Aug 17


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