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)

Our purpose was to determine whether the chronic increase in plasma volume (PV), resulting from heat exposure (HE) and exercise training (ET), was due only to elevated rectal temperature (Tre) or whether there were additional nonthermal factors related to the exercise. Eight men were divided into two groups. The HE group sat for 2 h/day (Tdb = 42 degrees C, 93% rh) for 8 consecutive days; Tre was raised by 1.72 +/- 0.04 degrees C to 38.5 degrees C each day. The ET group rode a bicycle ergometer for 2 h/day for 8 days (Tdb = 25 degrees C, 60% rh) at a load (60-65 Vo2max) that gave the same area under their Tre curve. PV increased by 177 ml (4.9%, P less than 0.05) in the HE group and by 427 ml (12.0%, P less than 0.05) in the ET group. This exercise-induced hypervolemia was associated with thermal factor(s) that contributed 40% and nonthermal factors that accounted for the remaining 60%. Some nonthermal, exercise-induced factors were twofold greater increases in plasma osmotic and vasopressin levels during exercise, and a fivefold increase in resting plasma protein (albumin) content.
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PMID:Role of thermal and exercise factors in the mechanism of hypervolemia. 699 62

To investigate the time course and mechanism of the increase in blood volume (BV) during isotonic exercise training, blood hemoglobin, hematocrit, and plasma volume (PV), osmotic, electrolyte, renin activity (PRA), vasopressin (AVP), and protein fractions were measured periodically in eight trained men 20-22 yr (Vo2max = 57 ml . min-1 . kg-1) before, during, and after ergometer exercise training (approximately 160 W, 65% Vo2max) for 2 h/day for 8 days. During training, plasma total osmolar and albumin contents increased to maintain a constant plasma osmolality and protein concentration during PV expansion. After training, BV increased by 457 ml (+8.1% P less than 0.05), due to an increase in PV of 427 ml (+12.1%, P less than 0.05); red cell volume was essentially constant (delta = +30 ml, NS). Plasma hypervolemia during training was associated with two major factors: 1) a ninefold elevation in PRA and AVP during exercise that facilitated Na+ and H2O retention, and 2) a progressive, chronic increase in plasma albumin content that provided increased H2O-binding capacity for the blood. Thus an efficient procedure for increasing PV is the daily performance of high-intensity isotonic leg exercise (65% Vo2max) for 2 h/day.
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PMID:Exercise training-induced hypervolemia: role of plasma albumin, renin, and vasopressin. 699 63

Despite numerous studies which have characterized the regulation of antidiuretic hormone (ADH), the role of volume in governing ADH release remains incompletely defined. Most studies have examined the quantitative effects of hypovolemia on arginine vasopressin (AVP). In contrast, few have assessed the role of hypervolemia on AVP regulation. Furthermore, there are no data to date on the effect of acute isoosmotic volume expansion on plasma AVP in man. The successful characterization of the water immersion model (NI) and the demonstration that it induces an acute central volume expansion without changes in plasma composition commended its utilization in the present study. Twelve normal subjects were studied after 14 h of dehydration on two occasions: control and during 4 h of NI. Blood was obtained every 30 min for AVP. AVP was unaltered during the control period. In contrast, there was a prompt and sustained suppression of AVP throughout NI (P < 0.05 vs. control). There were no concomitant changes in plasma osmolality. Since the changes in AVP occurred consequent to central volume expansion but in the absence of concomitant changes in plasma composition, the current data support the concept that acute isoosmotic central volume expansion in man results in a suppression of plasma AVP.
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PMID:Isoosmotic central blood volume expansion suppresses plasma arginine vasopressin in normal man. 700 2

Quantative data on plasma levels of antidiuretic hormone (ADH) in renal failure are limited. We measured predialysis plasma ADH levels using a double antibody radioimmunoassay in 14 patients with end-stage renal failure. Plasma ADH was inappropriately elevated in the majority of tested patients despite normal plasma osmolality, moderately elevated blood pressure, and hypervolemia. The etiology of increased plasma ADH in our population is unclear.
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PMID:Antidiuretic hormone in end-stage renal disease. 744 Aug 45

The influence of 1000 ml of 0.9% NaCl infusion induced hypervolemia on the water-electrolyte and hormonal balance was investigated in HBV-infected patients with chronic persistent hepatitis, chronic active hepatitis and compensated cirrhosis. All examined patients showed higher concentrations of vasopressin and atrial natriuretic peptide and the increased activity of RAA system before the trial. The induced hypervolemia caused the decrease of RAA system's activity and vasopressin concentration and increase of atrial natriuretic peptide's secretion, different in every group of patients. The latent deficiency of calcium and magnesium was found, too. The results showed that all determined patients had water-electrolyte and hormonal disorders, significantly increased in patients with chronic active hepatitis.
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PMID:[The influence of hypervolemia on the secretion of atrial natriuretic peptide, the renin-angiotensin-aldosterone system's activity and concentration of vasopressin, parathormone and calcitonin in hepatitis B virus infected patients with chronic liver diseases]. 759 80

The main objective of our study was to evolve a practical management protocol for neurosurgical patients with hyponatremia and natriuresis, based on their blood volume status and hematocrit. Twenty-one patients with hyponatremia and natriuresis and 3 control patients were studied. Patients with hyponatremia were categorized on the basis of their hematocrit, central venous pressure, and total blood volume. Group A consisted of patients with hypovolemia and anemia (16 patients); Group B patients had hypovolemia but no anemia (5 patients); Group C included those with hypervolemia (0 patients). Patients in Groups A and B received isotonic saline (> 50 ml/kg/d) and oral salt (12 g/d). Additionally, those in Group A were transfused with 500 ml of whole blood. The end points in the study were 72 hours after entry or two consecutive serum sodium values of > 130 mEq/L, whichever was earlier. Hyponatremia was corrected in all the patients within 72 hours (1 patient, < 24 h; 13 patients, < 48 h; and 7 patients, < 72 h). We conclude that most neurosurgical patients with hyponatremia and natriuresis have hypovolemia, with or without anemia. Fluid and salt replacement and a blood transfusion rather than fluid restriction often results in the correction of the hyponatremia. Our findings offer indirect evidence to support the hypothesis that in most of these patients, hyponatremia is caused by cerebral salt wasting syndrome, rather than the syndrome of inappropriate secretion of antidiuretic hormone.
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PMID:Management of neurosurgical patients with hyponatremia and natriuresis. 817 88

Carbamazepine (CBZ) has been reported to have an antidiuretic action, though it is not known how it produces this effect. This is a well recognized complication of CBZ therapy in adults. However this syndrome has been rarely observed in childhood. We present an epileptic child with fluid overload due to CBZ treatment who was referred with chest pain and cardiomegaly. Our patient developed fluid retention with cardiomegaly during treatment with CBZ alone at a normal dose and for a short time. To our knowledge this is the first case of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) due to CBZ therapy which has been observed to be associated with cardiomegaly.
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PMID:Fluid retention and cardiomegaly associated with carbamazepine in an epileptic child. 831 22

In congestive heart failure (CHF), a variety of compensatory mechanisms such as activation of sympathetic nervous system, renin-angiotensin system and vasopressin, facilitate water and sodium retention and increase circulating blood volume, which primarily improve systemic perfusion. However, hypervolemia sometimes induces pulmonary edema and afterload elevation, resulting in a further decrease in cardiac output. Diuretics are administered in patients with CHF to cut this vicious cycle by reducing blood volume. Evaluation of hemodynamic states is important in patients with severe CHF, since an excessive reduction in preload could critically decrease cardiac output. Among conventional diuretics, loop diuretics is the most potent and widely used for management of CHF. Inhibition of such compensatory mechanisms such as angiotensin-converting enzyme inhibitors and atrial natriuretic peptide-related agents is shown to exert natriuretic and desirable hemodynamic effects in CHF and is among candidates for future diuretics.
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PMID:[Progress in management for heart failure: diuretics]. 833 95

The atrial natriuretic peptide (ANP) is part of a new family of cardiac hormones regulating water and salt homeostasis. Besides acting as a blood pressure-lowering agent, it also exerts potent natriuretic and diuretic effects. ANP can be considered an endogenous antagonist of the reninangiotensin-aldosterone system and the antidiuretic hormone. One of the roles of ANP is to protect the body against fluid overload: it decreases intravascular fluid volume, which in turn diminishes cardiac secretion of ANP. The pharmacokinetic parameters of ANP reported in the literature vary widely. In general, ANP rapidly disappears from plasma with a high total body clearance. This is in agreement with the short-lived effects of the hormone. The actions of ANP have led to efforts to use this peptide hormone in the treatment of various cardiovascular disorders such as hypertension and congestive heart failure. Intravenous ANP administration indeed resulted in beneficial effects in these disorders. However, the peptide nature of ANP and its rapid elimination from the circulation limit its suitability as a drug. More promising is the development of long-acting ANP analogues and inhibitors of ANP degradation. Proper understanding of ANP pharmacokinetics is essential for the clinical use of these pharmacological agents.
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PMID:Atrial natriuretic peptide. An overview of clinical pharmacology and pharmacokinetics. 844 71

Because intravenous hydration is a commonly used first clinical effort to reduce preterm labor contractions, this review was initiated to determine whether the literature supports the effectiveness of this clinical strategy. An integrated, critical literature review was done by searching medical, nursing, public health, social, dissertation, and governmental databases to identify the studies relevant to this topic. Literature was chosen for review if it contained (1) objective data on the action of hydration on uterine contractility or (2) data on the clinical syndrome of threatened preterm labor. Research with animals has shown that rapid fluid administration blocks the central release of antidiuretic hormone and oxytocin through blood volume expansion, left atrial distention, and the resulting Henry-Gauer reflex, which thus alters uterine activity. Only four studies have been published that examined the effects of hydration for stopping labor. The effect of hydration was not significantly different from that of bedrest or of tocolytics in any of those studies. In all of them, time appears as an uncontrolled covariant. Although the consequences of hypervolemia might be expected to affect uterine contractions, there is no published evidence that pregnancies have been prolonged through the use of hydration. Hydration has rarely been studied as a single therapy in the prevention of preterm delivery. Caution concerning the use of intravenous hydration is advised by many authors reviewed, because if tocolytic drugs are administered after initial intravenous hydration with large amounts of fluids, the risk for pulmonary edema increases.
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PMID:Should intravenous hydration be the first line of defense with threatened preterm labor? A critical review of the literature. 891 39


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