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 Authors studied the effects of e.v. Salbutamol evaluating the acute "in vivo" variations of acid-base and hydro-electrolitic balance in 16 chronic obstructive lung patients undergoing e.v. drug administration, and also ionic variations "in vitro" of venous blood samples incubated and tonometrated with the drug. The results "in vivo" do not show variations of acid-base equilibrium (paO2, paCO2, pH, HCO3-); whereas diminution of haematocrit (Ht), rise of urinary osmolarity and variations of hydro-electrolitic balance (Na+, K+, Cl-) are demonstrated. The results "in vitro" do not show considerable variations on ionic assessment. These data, according to the other latest result, indicate the possible role of haemodilution. We think that the explanation of these phenomena could be a modification of renal water and electrolytes reabsorption, likely under the influence of antidiuretic hormone (ADH), stimulated in the hypothalamus and activated also by the beta-stimulant drug at tubular cell receptors.
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PMID:[Changes in the acid-base and water-electrolyte balance induced by salbutamol. "In vivo" studies in patients with chronic broncho-pulmonary disease and "in vitro" by tonometry of venous blood]. 3 12

H+ extrusion by the isolated skins of two amphibia, Rana ridibunda and Bufo bufo, was studied in order to test for the presence of exchange mechanisms of the type Na+/H+ and Cl-/HCO3-, which have been described in several epithelial structures. The preparations were mounted in chambers of the Ussing type, so that the short-circuit current could be used as a function of Na+ transport and the pH-stat techinique was utilize to determine the rates of H+ extrusion under different experimental conditions. The conditions were either the withdrawal of the ions intervening the mentioned exchanges (Cl- or Na+), or the addition of drugs with well-known effects on Na+ up-take and transport (antidiuretic hormone and amiloride). In the frog skin, H+ excretion was detected in solutions containing either Cl- or SO4-2-, with identical rates. Again, Na+ substitution by Mg-2+ had no effect on H+ excretion rates, neither did the suppression of Na+ influx by amiloride or its stimulation by antidiuretic hormone. These experiments were repeated with similar results in gland-free preparations of the epidermis of frog skin separated from the corion by the action of collagenase. Experiments in toad skin that H+ excretion could not be detected whan Cl- was present in the outer medium, but became apparent if an impermant anion, SO4-2-, was used. This observation is compatible with the existence of an exchange mechanism of the type Cl-/HCO3-. Secondly, in these preparations H+ extrusion increased after stimulation with antidiuretic hormone and decreased when amiloride was used or when Na+ was substituted by Mg+, suggesting that a least a fraction of the total H+ efflux is linked to Na+ influx. In the isolated frog skin this mechanism does not seem to be operative.
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PMID:The excretion of hydrogen ion by the isolated amphibian skin: effects of antidiuretic hormone and amiloride. 23 91

We evaluated demeclocycline and lithium therapy in 10 patients with the syndrome of inappropriate secretion of antidiuretic hormone. Despite severe water restriction, all patients had hyponatremia (mean +/- S.E.M. serum sodium of 122 +/- 1.1 meq per liter) and elevated urine osmolality (744 +/- 59 mOsm per kilogram) before treatment. Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients. In three patients given lithium carbonate (900 mg daily) the serum sodium concentration, urine osmolality and urine volume were unchanged; since two patients had adverse central-nervous-system symptoms during lithium therapy, further study of this agent was abandoned. A patient with an unusual 22-year history of the syndrome was unresponsive to lithium, whereas long-term treatment with demeclocyline was markedly effective. Demeclocycline is superior to lithium in the treatment of the syndrome and may obviate the need for severe water restriction.
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PMID:Superiority of demeclocycline over lithium in the treatment of chronic syndrome of inappropriate secretion of antidiuretic hormone. 41 37

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was 'unmeasured' (Na+ + K+ - [Cl- + HCO3- + PO4(3-)]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.
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PMID:Natriuresis in rats acutely depleted of chloride. 60 61

Since recent investigations have shown elevated urinary PGE2 and polyuria in hypokalemic animals which were reversed by PG synthesis inhibition with indomethacin, studies were undertaken to examine the effects of extracellular [K+] on renomedullary PG production in vitro. Slices of rabbit and human renal papilla were incubated in Krebs-Ringer HCO3- buffer, 95% O2-5% CO2, glucose 10 mM, HSA 4 gm/100 ml, for 30 min at 38 degrees C, with and without 1-14C-AA (10 micrometer). Measurments were made of total endogenous iPGE2 and iPGF2alpha production and radioactive AA leads to PGE2. In rabbit renal medulla values for iPGE2 (nmol/gm/30 min) were 252 +/- 20 at [K+] 0; 182 +/- 17 at [K+] 2.5 mEq/L; 163 +/- 18 at [K+] 5.5; and 129 +/- 17 [K+] 9.0 (p less than 0.005). iPGF2alpha was unaltered by changes in media potassium concentrations (6.8 +/- 0.9 nmol/gm/30 min at [K+] 0 and 6.2 +/- 0.8 at [K+] 9.0 MEq/L). In the human renal medulla iPGE2 was 9.5 +/- 1.6 nmol/gm/30 min at [K+] 0; 5.0 +/- 0.7 at [K+] 2.5 mEq/L; 5.3 +/- 0.3 at [K+] 5.5; and 4.6 +/- 1.0 at [K+] 9.0 (p less than 0.05). AA leads to PGE2 (nmol/gm/30 min) was 3.21 +/- 0.92 at [K+] 0; 2.47 +/- 0.57 at [K+] 2.5 mEq/L; 1.30 +/- 0.30 at [K+] 5.5; and 0.76 +/- 0.4 at [K+] 9.0 in rabbit medulla (P less than 0.005). It is postulated that direct stimulation of papillary PGE2 biosynthesis by low extracellular [K+] impairing the cAMP-generating response to vasopressin could represent the initial event in the pathogenesis of vasopressin-resistant polyuria.
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PMID:Renal biosynthesis of prostaglandin E2 and F2alpha: dependence on extracellular potassium. 71 2

The usual treatment for recurrent syndrome of inappropriate secretion of antidiuretic hormone has been fluid restriction. Recently White and Fetner described an adult with SIADH successfully managed with lithium carbonate. Described here is a child with recurrent SIADH who was diagnosed as having an acute hyponatremic episode and who then relapsed twice in a two-month period while chronic fluid restriction was attempted. He has now been maintained on 300 mg/day of lithium carbonate and is asymptomatic with normal serum sodium concentration and urine osmolalities. Lithium appears to be effective in the management of recurrent SIADH and may allow control in a patient who cannot comply with long-term fluid restriction.
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PMID:Treatment of recurrent syndrome of inappropriate secretion of antidiuretic hormone with lithium. 83 44

A case of a 76-year-old man with the syndrome of inappropriate secretion of antidiuretic hormone (ADH) is discussed. The patient was initially treated with fluid restriction followed by the administration of hypertonic saline. After failure to achieve rapid correction of the condition and continued lethargy and muscle weakness in the patient, a trial with lithium carbonate 300 mg three times daily via nasogastric tube was initiated. This resulted in a prompt reversal of the hyperosmolar state and improvement in electrolyte balance. However, despite the apparent success in treating his inappropriate ADH, the patient expired as a result of a massive cerebral vascular accident. The potential benefit of using lithium in the treatment of the syndrome of inappropriate secretion of ADH, and possible mechanisms of action, are reviewed.
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PMID:Lithium carbonate treatment in the syndrome of inappropriate secretion of antidiuretic hormone. 92 Jul 46

Lithium carbonate, useful in the treatment of manic-depressive disorders, can produce nephrogenic diabetes insipidus. The drug, therefore, has been used to facilitate renal waster excretion when severe hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion. Symptomatic dilutional hyponatremia developed in a patient with pulmonary carcinoma whom we treated. Lithium carbonate was administered and renal sodium wasting, hypovolemia, and hypotension occurred. Hyperkalemia was also observed, and since adrenal steroid levels were not decreased, impairment of distal tubular function was suggested. Lithium carbonate blocks antidiuretic hormone effect by decreasing collecting duct cyclic adenosine monophosphate generation. These observations suggest that more generalized inhibitory effects on renal tubular function may also result from its use. An alternative drug, demeclocycline, may be preferable.
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PMID:Severe sodium depletion syndrome during lithium carbonate therapy. 93 81

Recent studies have shown that chronic hypotonic volume expansion (HVE) induced by administration of vasopressin and water stimulates distal hydrogen ion secretion and thereby (a) permits dogs with HCl-acidosis to restore acid-base equilibrium to normal despite continued acid feeding and (b) permits normal dogs to conserve filtered bicarbonate quantitatively despite the natriuresis induced by water retention. To examine whether these effects of chronic HVE are mediated by augmented mineralocorticoid secretion, urinary and plasma aldosterone levels were monitored during prolonged administration of vasopressin. In HCl-fed animals, the HVE-induced rise in plasma [HCO3] (from 13.8 to 21.3 meq/liter) was associated with a rise in aldosterone excretion from 0.45 to 0.88 mug/day (P less than 0.02). In normal animals, in which plasma [HCO3] remained stable during HVE (21.9 vs. 20.0 meq/liter), aldosterone excretion rose from 0.51 to 2.28 mug/day (P less than 0.02) and plasma aldosterone concentration rose from 8.1 to 39.8 ng/100 ml (P less than 0.01). Vasopressin and water were also administered to adrenalectomized animals maintained on glucocorticoids and a slightly subphysiologic replacement schedule of mineralocorticoids. In the HCl-fed adrenalectomized group, plasma [HCO3], instead of rising to normal, showed no significant change (16.9 vs. 15.0 meq/liter). In the non-HCl-fed adrenalectomized group, plasma [HCO3], rather than remaining stable, fell significantly (20.3 vs 16.5 meq/liter, P less than 0.1). Two conclusions can be drawn from this study: (a) the well-known inhibitory effect of volume expansion on aldosterone secretion can be overridden by a potent stimulatory effect on the adrenal produced by severe chronic hypotonicity, and (b) the response of plasma [HCO3] observed during severe chronic HVE is mediated by augmented mineralocorticoid secretion. These findings, furthermore, offer a possible explanation for the puzzling observation that plasma [HCO3] in patients with the syndrome of inappropriate antidiuretic hormone secretion is maintained at normal levels even in the face of severe hyponatremia.
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PMID:The critical role of the adrenal gland in the renal regulation of acid-base equilibrium during chronic hypotonic expansion. Evidence that chronic hyponatremia is a potent stimulus to aldosterone secretion. 99 40

Lithium, an established inhibitor of antidiuretic hormone action, was used (as the carbonate salt) to treat a patient with the syndrome of inappropriate secreation of antidiuretic hormone. The patient was studied by balance technics, and after a stablized hyponatremic state developed, 0.9 g of lithium carbonate was administered daily. A prompt water diuresis ensued, with correctionof hyponatremia in two days. Discontinuation of the drug resulted in a gradual return of the hyponatremic state. No change in urinary cyclic AMP occurred during the period of lithium effect. Lithium carbonate may be an effective treatment for both the acute and the chronic forms of the syndrome.
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PMID:Treatment of the syndrome of inappropriate secretion of antidiuretic hormone with lithium carbonate. 111 Jul 24


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