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. The proposition that changes in renal calcium excretion during vasopressin administration are positively correlated with concurrent changes in urine hydrogen ion concentration was tested by administration of vasopressin into twelve conscious diuresing sheep receiving either alkalinizing or acidifying infusions. 2. Vasopressin-induced antidiuresis in sheep with alkaline urine was associated with significant increases in urinary pH and decreases in the rate of calcium excretion whereas antidiuresis in sheep with acid urine was associated with significant decreases in urinary pH and no consistent effect on calcium excretion. 3. Magnesium excretion increased during vasopressin administration in most experiments regardless of urinary pH changes. 4. Vasopressin administration did not significantly alter the rate of excretion of sodium, potassium, chloride and phosphate or the rates of sodium, potassium, chloride, inulin, para-aminohippurate and osmolal clearance in sheep with either acid or alkaline urine. Potassium excretion and clearance in sheep with alkaline ruine was higher than that of sheep with acid urine during vasopressin infusion. 5. The results support the hypothesis that changes in renal tubular hydrogen ion concentration or bicarbonate concentration caused by water reabsorption from the collecting duct and possibly the late distal tubule could be part of the explanation for changes in renal calcium excretion which occur during vasopressin-induced antidiuresis.
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PMID:Renal calcium and magnesium excretion during vasopressin administration into sheep with acid or alkaline urine. 4 39

30 patients on long-term lithium therapy have been studied. The results are presented of the urinary concentrating ability after water deprivation and the intranasal administration of vasopressin, of the simultaneous determination of glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), of the minimal urine pH after an oral dose of ammonium chloride, and of the urinary beta-2-microglobulin excretion. Mean urine concentration (+/- SEM) after 22 hr water deprivation (= Uosm) amounted to 854 +/- 22 mOsm/kg H2O, mean GFR was 101 +/- 4 ml/min, mean ERPF 360 +/- 18 ml/min, and mean minimal urine pH 4.95 +/- 0.06. In 8 out of 30 patients there was polyuria. In these 8 patients the values were 778 +/- 51 mOsm/kg H2O, 113 +/- 6 ml/min, 415 +/- 33 ml/min and 4.99 +/- 0.08, respectively. Serum levels of beta-2-microglobulin and lysozyme and the urinary excretion of beta-2-microglobulin were normal in all patients. No correlation was established between Uosm and the serum lithium concentration during the test (0.8 +/- 0.05 mmoles/l) nor between Uosm and the average serum lithium level during treatment (0.79 +/- 0.03). GFR was only correlated with age. It was found that administration of indomethacin during the concentration test increased Uosm in these patients. The results suggest that, given proper dosage and surveillance, long-term treatment with lithium is not likely to cause disturbances in renal function.
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PMID:A renal function study in 30 patients on long-term lithium therapy. 4 7

Intrarenal infusion of somatostatin in anesthetized dogs produced a prompt increase in urine flow in association with a decrease in urinary osmolality and an increase in free water clearance. These changes occurred in the absence of changes in arterial pressure, renal plasma flow, osmolar clearance, electrolyte excretion or cyclic AMP excretion. The diuretic effect occurred primarily in the infused kidney indicating a direct intrarenal action rather than suppression of vasopressin secretion. This diuretic action of somatostatin may result from inhibition of the action of vasopressin on the renal medulla but other possible mechanisms cannot be excluded.
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PMID:An intrarenal effect of somatostatin on water excretion. 4 71

Ethanol (9%) decreases the potential difference across the toad bladder when present at the mucosal surface, the short-circuit current was unchanged. The electrical resistance decreased indicating a change in ion movements across the bladder. Unidirectional 22Na and 36Cl flux measurements showed an increase in the movement of Cl, but no change in Na. The vasopressin-induced increase in Na transport (natriferic response) was also unaffected by the presence of ethanol. It is suggested that ethanol may be altering the apical tight junctions and affecting an anion selective pathway. The hydro-osmotic response of the toad bladder to vasopressin was decreased by 70% in the presence of 3% ethanol. The hydro-osmotic action of cyclic adenosine monophosphate was also inhibited by ethanol, indicating an action subsequent to the endogenous formation of this nucleotide. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. The vasopressin-induced increase in diffusional water flow was similarly reduced. Osmotic water movements across glutaraldehyde and N-ethylmaleimide-"fixed" vasopressin-stimulated bladders were also decreased in the presence of ethanol. However, 3% ethanol had no effect on osmotic water transfer across artificial collodion membranes. Ethanol, therefore, probably interacts with the bladder membrane. The Ktrans (permeability coefficient) of ethanol and water is increased by vasopressin. suggesting that their movement is through similar pathways. It is suggested that ethanol empedes the flow of water across the toad bladder by facilitating a physicochemical interaction between the membrane "pore" and the water molecules.
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PMID:Effects of ethanol on the permeability of toad urinary bladder epithelium. 5 35

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.
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PMID:Severe hyponatraemia. A study of 17 patients. 7 64

Colchicine, podophyllotoxin and vinblastine have been found to inhibit the action of vasopressin on water movement in the toad urinary bladder. Tubulin is the major colchicine binding component of toad bladder epithelial cells, accounting for approximately 3.3% of the total cell protein. More than 99% of the tubulin is found in the soluble fraction after sonication, the remainder is in the particulate fraction. Similar to the characteristics of the binding of colchicine to tubulins from other sources, the binding of colchicine to toad bladder tubulin is temperature- and time-dependent, is inhibited competitively by podophyllotoxin (Ki= 5.5 x 10(-7)m), and has a binding constant of 1 X 10(6) liters/mole at 37 degrees. Binding activity decays according to first-order kinetics and is stabilized by vinblastine. The characteristics of the interactions of colchicine and podophyllotoxin with epithelial cell tubulin in vitro closely parallel the ability of these drugs to inhibit the response to vasopressin in vivo. These results, coupled with those of functional and morphological studies, support the view that the ability of these drugs to affect vasopressin-induced water movement across toad bladder epithelial cells is related to the depolymerization of cytoplasmic microtubules.
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PMID:Evidence for involvement of microtubules in the action of vasopressin in toad urinary bladder. II. Colchicine binding properties of toad bladder epithelial cell tubulin. 9 70

The brain vasculature, especially capillaries, may function in a very dynamic fashion under neuroendocrine control to regulate the internal environment of the brain. This is exemplified by new observations on the regulation of brain water permeability using the tracer H215O in vivo in adult rhesus monkeys. These studies reveal that brain water permeability, and hence brain water content and volume, are, at least in part, under the influence of the central noradrenergic system and centrally released vasopressin.
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PMID:Central neuroendocrine regulation of brain water permeability. 9 63

Two patients with the syndrome of inappropriate secretion of antidiuretic hormone were studied in a metabolic ward during treatment with 1.2 g demeclocycline daily. In both patients, demeclocycline treatment led to increased renal water excretion with consequent correction of hyponatremia and hypo-osmolality. Three episodes of reversible deterioration in glomerular filtration rate developed in these patients. Each episode was accompanied by clinical evidence of extracellular fluid volume contraction, and on each occasion there was an inappropriate natriuresis with daily urinary sodium excretion remaining above 50 mEq. Although demeclocycline effectively reverses the electrolyte abnormalities of this syndrome, the potentially dangerous side effects that may develop exclude the routine usage of the drug.
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PMID:Renal function during treatment of inappropriate secretion of antidiuretic hormone with demeclocycline. 10 Apr 73

The effect of prostaglandin synthesis inhibition on the redistribution of renal cortical blood flow in response to antidiuretic hormone (ADH) was examined using radioactive microspheres in water loaded, thiopental-anesthetized dogs. Microsphere injections were made during a control and an ADH infusion period (0.35 mU/kg/min following a 20 mU/kg bolus) both before and after indomethacin pretreatment (8 mg/kg intravenously). Urinary prostaglandin E2 (PGE2) excretion in each period was measured by gas chromatography-mass spectrometry. ADH caused a marked redistribution of flow toward inner cortical zones from 19 +/- 1 to 25 +/- 2 ml/min (mean +/- SE, p less than 0.01). Fractional flow to inner zones was also significantly increased. Indomethacin pretreatment had no effect on the ADH-induced redistribution (17 +/- 2 vs. 24 +/- 2 ml/min, p less than 0.01), although urinary PGE2 excretion was suppressed by indomethacin by 60%. It is concluded that prostaglandins do not mediate the redistribution of intrarenal blood flow accompanying ADH administration.
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PMID:Redistribution of intrarenal blood flow following ADH administration: lack of inhibition by blockade of prostaglandin in cyclooxygenase. 10 3

The effects of the antidiuretic hormone (ADH) on the renal excretion of urea and electrolytes were studied in sheep, subjected to water stress, before and after 36-hour fasting. The intravenous administration of synthetic lysine-vasopressin (L-VP) at the dose of 100 microgram per kg induced only a temporary, statistically insignificant, drop of the urinary urea outputs by the fed as well as fasting sheep. L-VP did not influence the excretion of sodium and potassium electrolytes either. It follows from the results that there are no differences in the renal response to ADH between the fed sheep and sheep that have fasted for 36 hours.
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PMID:[The effect of the antidiuretic hormone on the renal excretion of urea and electrolytes in fed and fasting sheep]. 10 79


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