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)

Polyuria and polydipsia developed in two cases during amphotericin B therapy for deep mycoses. Neither patient could concentrate his urine in response to water deprivation or exogenous vasopressin. Other causes of vasopressin-resistant nephrogenic diabetes insipidus were not present. Three months after amphotericin B therapy had been discontinued, concentrating ability improved toward normal. A third patient was further observed and demonstrated normal diluting capacity but impaired free-water reabsorption, suggesting a distal tubular defect consistent with nephrogenic diabetes insipidus. Four months after discontinuing therapy, renal concentrating ability was normal. Amphotericin B can induce a reversible form of nephrogenic diabetes insipidus.
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PMID:Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy. 76 Jun 89

La3+ was used to assess the role of membrane-bound Ca2+ in the regulation of basal and antidiuretic hormone (ADH)-induced Na+ transport by the isolated toad urinary bladder. Na+ transport was monitored by means of a short-circuit current (Isc) device. Mucosal La3+ (0.5-5 mM) increased Isc, while serosal La3+ (5 mM) produced a biphasic response (stimulation followed by inhibition). The stimulatory effects of La3+ were additive when present on both sides and were suppressed by mucosal amiloride or serosal ouabain. The action of mucosal La+ was reversible but the inhibition produced by serosal La3+ was not. In the presence of serosal La3+ the natriferic effect of ADH was abolished, but Theophylline, dibutyryl-cAMP, Amphotericin B, mucosal La3+, mucosal low pH, and phospho(enol) pyruvate, were able to increase Isc. These results suggest that Ca2+ binding sites in apical and basolateral membranes may play a key role in the modulation of both basal and ADH-induced Na+ transport. Serosal La3+ apparently inactivates the hormone-receptor interaction and/or the link between the ADH-receptor complex and the activation of adenylate cyclase, but does not interfere with the operation of the Na+ "pump", the basal activity of adenylate cyclase or any of the intracellular events that mediate the effect of ADH on Na+ transport.
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PMID:Possible role of Ca2+-binding sites in the regulation of Na+ transport in toad urinary bladder. 242 67

Capsule-deficient Cryptococcus neoformans (CN-CD) infection is very rare. The authors recently experienced the case of CN-CD infection with the complication of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a 83 year old woman. She was admitted to our hospital with the complaints of fever and general fatigue on June 10, 1987. At the time of admission, there were no abnormal findings except a mildly lowered consciousness level on physical examination, there were no abnormal neurological finding nor meningeal signs. Laboratory data revealed a mild leukocytosis and hyponatremia. Chest X-P showed a few small nodular shadows scattered in both lungs. Antibiotics therapy was of no help and hyponatremia became worse. Then with the suspicion of SIADH, Demeclocycline was administered and limitation of water intake was decreased and hyponatremia improvement was used. Yeast-like fungi was detected in the venous blood culture and in the cerebrospinal fluid (cell count: 252/3) CN-CD by India-ink preparation and bacteriological nature were determined. We made a diagnosis of sepsis and meningitis by CN-CD accompanied with SIADH. In spite of Miconazole administration intravenously and intrathecally, she died 2 months after admission. The minimal inhibitory concentration (micrograms/ml) of antibiotics against the isolated CN-CD was as follows: Amphotericin B: 0.78, 5-PC: 1.56, Miconazole less than or equal to 0.05, Nystatin: 25, Ketoconazole: 0.78.
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PMID:[A case of sepsis and meningitis due to capsule-deficient Cryptococcus neoformans with SIADH]. 269 39

Amphotericin B (AmB) increased unidirectional Na transport and net transcellular sodium movements across the skin of the frog, Rana pipiens, when added to the solution bathing the corium side, but not from the outer epidermal surface. The AmB response was prevented with pretreatment with amiloride, ouabain and mucosal sodium substitution. Alteration in pH markedly reduced the permeability changes induced by AmB. AmB did not interfere with the increase in sodium transport induced by antidiuretic hormone. The present study demonstrates that AmB interacts with the skin of the frog, Rana pipiens, from the corium side specifically increasing transepithelial sodium transport. The increase in transport apparently occurs through the existing sodium pathway.
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PMID:Alteration of membrane permeability by amphotericin B. 285 29

Incorporating amphotericin B into liposomes was reported to decrease amphotericin B toxicity without a concomitant loss of antifungal efficacy. We formulated an alternative emulsion-based delivery system for amphotericin B and compared it with Fungizone. The maximal tolerated dose (MTD) in mice was 1 mg of Fungizone/kg; however, the MTD was greater than 9 mg of the Intralipid emulsion formulation/kg. The emulsion formulation and Fungizone were equipotent for treating systemic candidiasis in mice. Amphotericin B nephrotoxicity, as manifested by polyuria that was resistant to antidiuretic hormone, was markedly diminished when amphotericin B was administered as an emulsion to rats. Loss of potassium from human red blood cells was also reduced by formulating this agent within emulsions. The emulsion formulation extended the survival time of mice that had established Candida albicans infections, when compared with the Fungizone treatment. The efficacy and reduced toxicity of the amphotericin B emulsion are findings suggesting that the emulsion formulation is preferable to Fungizone.
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PMID:An emulsion formulation of amphotericin B improves the therapeutic index when treating systemic murine candidiasis. 318 18

1 Amiloride inhibits Na transport and short-circuit current (SCC) across the toad bladder. It is 1000 times more active at the mucosal than serosal surface. The lowest effective concentration was 10(-7)M.2. The inhibition was non-competitive with the sodium on the mucosal side of the bladder.3. Vasopressin, cyclic adenosine monophosphate (AMP) and aldosterone increased Na transport and SCC across the bladder and these effects were inhibited by amiloride.4. The antagonism of amiloride for vasopressin was non-competitive.5. Amphotericin B also increases Na transport across the bladder but its action was not changed by amiloride.6. Amiloride was without effects on SCC and diffusion potentials in bladders metabolically inhibited with CN(-) and iodoacetic acid (IAA).7. Neither plasma albumin, Ca(2+) nor adenosine triphosphate (ATP) altered the effects of amiloride.8. The only structural analogue of amiloride found to reduce SCC similarly was guanidine which was 1000 times less active. Pyrazine and a substituted pyrazine analogue were without effect. Neither guanidine nor the substituted pyrazine compound were competitive with amiloride.9. Amiloride had no effect on the osmotic permeability of the toad bladder either in the presence or absence of vasopressin.10. Na transport across the toad colon was also reduced by 10(-5)M amiloride at the mucosal surface.11. The possible mechanism of action of amiloride is discussed.
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PMID:Amiloride: a potent inhibitor of sodium transport across the toad bladder. 564 23