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 cirrhotic patient with acute bleeding from esophageal varices has less than a 50% chance of leaving the hospital alive; the outlook for survival is so poor that even desperate measures are worthwhile. Some traditional nonsurgical methods for the control of the bleeding are either ineffective at worst or temporary at best. Balloon tamponade is not recommended at all, but intravenously administered vasopressin may be helpful in allowing the necessary diagnostic investigations to be completed. Most important at this stage are the measures necessary to improve the general status of the patient--restoration of blood volume with fresh blood, prevention of ammonia intoxication, support of the liver, correction of metabolic alkalosis and treatment of the hyperdynamic state with digitalis and cardiotonic drugs. Controlling the bleeding is not the greatest problem--the greatest problem is achieving survival of a critically ill patient who undergoes a formidable operation (e.g., variceal ligation stops the bleeding, but is itself an operation of considerable magnitude). In our hands emergency shunting is the best treatment providing a definitive procedure with the highest 10-year survival rate and the lowest complication rate.
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PMID:Emergency treatment of variceal hemorrhage. 38 92

Diuretics have long been used to lower blood pressure in hypertensive patients or to control body fluid and electrolyte homeostasis in diseases such as congestive heart failure, chronic renal failure or cirrhosis. The initial response to diuretics is a negative sodium and fluid balance. The diuretic-induced loss of salt and water activates several hormonal systems such as vasopressin, the renin-angiotensin-aldosterone system or the sympathetic nervous system which tend to compensate for the changes in sodium and water balance. This neurohormonal response may have important clinical implications. Thus, the activation of the renin-angiotensin-aldosterone cascade appears to be partially responsible for the flat dose-blood pressure response curve of thiazides in hypertensive patients. It may also be responsible for the difference between responders and non-responders to diuretic therapy and for the development of side-effects such as hypokalaemia, metabolic alkalosis or hyponatraemia. There are several ways to prevent the undesirable consequences of the neurohormonal responses to diuretics. The first is to use low doses of these agents. It is also possible to combine them with agents that block the activity of the renin-angiotensin-aldosterone system such as ACE inhibitors or in combination with drugs that reduce aldosterone secretion such as calcium antagonists. The development of drugs able to enhance urinary sodium excretion and to reduce simultaneously the activity of the renin-angiotensin-aldosterone system may offer a new interesting alternative. This might perhaps be achieved in the future with the administration of neutral endopeptidase inhibitors which interfere with the enzymatic degradation of atrial natriuretic peptide.
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PMID:Neurohormonal consequences of diuretics in different cardiovascular syndromes. 136 43

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

Renal electrolyte and net acid excretion were characterized during generation and maintenance of hypochloremic metabolic alkalosis in a ruminant model. Two phases of renal response with regard to sodium and net acid excretion were documented. An initial decrease in net acid excretion was attributable to increase in bicarbonate excretion with associated increase in sodium excretion. As the metabolic disturbance became more advanced, a second phase of renal excretion was observed in which sodium and bicarbonate excretion were markedly decreased, leading to increase in net acid excretion and development of aciduria. Throughout the metabolic disturbance, chloride excretion was markedly decreased; potassium excretion also decreased. These changes were accompanied by increase in plasma renin and aldosterone concentrations. There was apparent failure to concentrate the urine optimally during the course of the metabolic disturbance, despite increasing plasma concentration of antidiuretic hormone.
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PMID:Renal net acid and electrolyte excretion in an experimental model of hypochloremic metabolic alkalosis in sheep. 224 Jul 96

Vanadate has been used in many cellular systems to elucidate mechanisms of enzyme action. Vanadate inhibits Na-K adenosine triphosphatase (ATPase) activity in many tissues. In isolated collecting tubule it inhibits sodium transport and vasopressin-stimulated water flux, the latter presumably distal to cyclic AMP formation. Depending upon the tissue studied, vanadate also stimulates a variety of cellular reactions including adenylate cyclase, glucose oxidation and glycogen synthesis. We studied the effect of varying concentrations of vanadate on N-ethylmaleimide (NEM)-sensitive ATPase activity in microdissected segments of rat nephron. In proximal convoluted tubule and in cortical, medullary and papillary collecting ducts vanadate had no effect on enzyme activity. In medullary and cortical thick ascending limbs, however, vanadate significantly stimulated NEM-sensitive ATPase activity (medullary thick ascending limb, 241 +/- 14 pmol/mm/hr vs. 531 +/- 74 pmol/mm/hr; control vs. (1 mM) vanadate, respectively; n = 14, P less than 0.01). The stimulatory effect of vanadate on NEM-sensitive ATPase activity was present at 5 microM vanadate, a concentration that inhibited Na-K ATPase activity approximately 80%. Metabolic acidosis also stimulated enzyme activity in the thick ascending limb, and the effect of vanadate was not additive. Metabolic alkalosis had no effect on NEM-sensitive ATPase in the thick ascending limb, but the stimulatory effect of vanadate was still seen. These data document that the NEM-sensitive ATPase in thick ascending limb is different from that found in other nonmammalian proton secretory epithelia which are vanadate inhibitable. The results with vanadate plus metabolic acidosis suggest that both are acting via the same mechanism.
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PMID:Vanadate stimulates the N-ethylmaleimide-sensitive adenosine triphosphatase in rat nephron. 252 98

Alkaline secretion of the duodenal mucosa is thought to be an important protective mechanism against luminal acid. This study was designed to investigate the role of acid base balance and mucosal blood flow for duodenal alkaline secretion in an in vivo preparation. Segments of proximal duodenum of anaesthetised New Zealand white rabbits were canulated and perfused in situ. Alkaline secretion (pH-stat method), mucosal blood flow, arterial pO2, pCO2 and HCO-3 were measured. We have found that metabolic alkalosis and glucagon led to a significant increase in alkaline secretion, while metabolic acidosis and vasopressin significantly reduced it. Mucosal blood flow was significantly changed under glucagon and vasopressin.
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PMID:Role of acid base balance and mucosal blood flow in alkaline secretion of rabbit duodenum. 254 Jun 20

Chronic chloride depletion alkalosis in dogs causes a lowered osmotic threshold and increased sensitivity for vasopressin (AVP) release. Since AVP release and drinking behavior normally are closely associated over a narrow range of changes in plasma osmolality (Posm), we investigated whether alkalotic dogs would also show an altered responsiveness to the dipsogenic effects of angiotensin II (ANG II) and osmotic stimuli. Dogs made chronically alkalotic by a combination of chloride-free diet and furosemide injections developed polydipsia in the absence of any increase in solute intake and in the presence of a significant reduction in Posm. The animals were chronically hypochloremic, hyponatremic and hypokalemic, and appeared to be extracellular fluid (ECF) contracted. Plasma renin activity (PRA) was 10-fold higher in alkalotic dogs than controls. When Posm was increased by a slow 2 hr infusion of hypertonic sodium sulfate, alkalotic dogs were found to have a significantly lower osmotic threshold for inducing drinking (289.8 +/- 1.1 mOsm/kg/H2O vs. 305.1 +/- 1.3 mOsm/kg/H2O in controls), but the slope or sensitivity of the water intake/Posm relationship was not significantly different. Finally, compared to normal animals, alkalotic dogs were unresponsive to the dipsogenic effects of IV ANG II. These data indicate that the central mechanisms which mediate drinking in response to cellular and extracellular thirst stimuli are altered in chronic metabolic alkalosis.
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PMID:Altered drinking responses in dogs with chronic metabolic alkalosis. 285 45

Different rates of alkaline secretion and their effect on acid tolerance were investigated in segments of proximal duodenum of anaesthetized New Zealand white rabbits in situ. Metabolic alkalosis and glucagon led to a significant increase in alkaline secretion, while metabolic acidosis, vasopressin and furosemide significantly reduced alkaline secretion. Mucosal blood flow was significantly increased by glucagon and decreased by vasopressin. Alkaline secretion after an acid challenge was significantly higher than preacid secretion in animals with metabolic alkalosis, glucagon and NaCl, whereas vasopressin reduced alkaline secretion significantly. No significant change was observed during treatment with furosemide or metabolic acidosis. After perfusion with acid, 51.8% of the villi showed superficial damage (stage 1) under control conditions. Damage was significantly reduced after administration of bicarbonate or glucagon, while NH4Cl, vasopressin or furosemide increased damage both quantitatively and qualitatively. There was a direct linear correlation between the degree of damage and alkaline secretion. The proximal duodenum showed considerably less damage than the distal segment. We conclude that a decrease in alkaline secretion is associated with a reduced tolerance of duodenal mucosa to luminal acid, whereas stimulation of alkaline secretion improves mucosal protection. These results support the hypothesis that alkaline secretion is an important factor in the protection of the duodenum against luminal acid.
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PMID:[Significance of alkali secretion in acid tolerance of the rabbit duodenum]. 343 85

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21

Some of the biochemical changes which occur at the menopause can be attributed to an increased rate of loss of bone but others cannot be explained in this way. Data, collected through literature search, are presented which suggest that the rise in plasma phosphate concentration at the menopause is not due primarily to increased breakdown of bone but rather to the following sequence of events: progesterone deficiency----respiratory hypoventilation----mild respiratory acidosis and hypoxia----compensatory metabolic alkalosis----altered carbohydrate metabolism----rise in plasma phosphate concentration. Increases in the concentration of many plasma constituents occur at the menopause, which appear to be due to fluid loss and haemoconcentration. A possible cause of these changes is a reduced secretion of vasopressin by the pituitary gland as a result of oestrogen deficiency. Increases in the fasting urinary excretion of phosphate, sodium and magnesium also occur at the menopause. These changes cannot be attributed to increased bone loss but could be due to the effects of oestrogen deficiency on circadian rhythms in the hypothalamus.
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PMID:Hypothesis. Biochemical changes at the menopause: possible role of the central nervous system. 639 28


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