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Research Article Free access | 10.1172/JCI106040

Effect of Adrenal steroid hormones on the response of the toad's urinary bladder to vasopressin

J. S. Handler, A. S. Preston, and J. Orloff

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Handler, J. in: JCI | PubMed | Google Scholar

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Preston, A. in: JCI | PubMed | Google Scholar

1Laboratory of Kidney and Electrolyte Metabolism, National Heart Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Orloff, J. in: JCI | PubMed | Google Scholar

Published May 1, 1969 - More info

Published in Volume 48, Issue 5 on May 1, 1969
J Clin Invest. 1969;48(5):823–833. https://doi.org/10.1172/JCI106040.
© 1969 The American Society for Clinical Investigation
Published May 1, 1969 - Version history
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Abstract

This study was designed to examine the effect of adrenal steroid hormones on the response of the toad bladder to vasopressin. Aldosterone enhanced the short-circuit current response, the osmotic water flow response, and the urea permeability response to vasopressin. Since aldosterone also enhanced the short-circuit current response and the osmotic water flow response to adenosine 3′,5′-monophosphate, the steroid effect on the bladder's response to vasopressin appears to be at a step beyond the stimulation of adenyl cyclase.

Indirect evidence was obtained that the effect of adrenal steroid hormones on the osmotic water flow response to vasopressin is mediated by a different hormone-tissue interaction than that mediating the effect of adrenal steroid hormones on sodium transport. In experiments with three different pairs of mineralocorticoid and glucocorticoid analogues, the former had a greater effect on short-circuit current, the latter on the osmotic water flow response to vasopressin. In addition, the spirolactone SC-14266 markedly inhibited the short-circuit current effect of dexamethasone and had little or no inhibitory effect on the dexamethasone enhancement of the osmotic water flow response to vasopressin. Aldosterone and dexamethasone stimulate the oxidation by the bladder of glucose-6-14C and depress the rate of oxidation of glucose-1-14C compared with glucose-6-14C. SC-14266 inhibited the effect of dexamethasone on the oxidation of glucose-6-14C but did not alter the effect of the steroid on the rate of oxidation of glucose-1-14C compared with glucose-6-14C, suggesting that the latter is a glucocorticoid effect and the stimulation of glucose-6-14C oxidation a mineralocorticoid effect. Under conditions in which aldosterone has produced a marked enhancement of short-circuit current and the permeability response to vasopressin, the steroid had no detectable effect on cell water content or on cell sodium, potassium, or chloride.

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