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J S Handler

Publications and source records attributed to J S Handler.

At least 127 records · Page 7Linked to original sources
PubMed1972

The effect of aldosterone on the accumulation of adenosine 3':5'-cyclic monophosphate in toad bladder epithelial cells in response to vasopressin and theophylline.

Vasopressin and theophylline both increase the content of adenosine 3':5'-cyclic monophosphate (cAMP) in epithelial cells of the urinary bladder of toads (Bufo marinus). Incubation of the tissue with 0.2 muM aldosterone markedly increases this response to the two agents; incubation for a similar time without steroid reduces the response. The permeability responses (sodium transport and water flow) of the intact tissue to vasopressin, theophylline, and exogenous cAMP are also considerably greater in bladders incubated with aldosterone than without. The results are interpreted as indicating that the foregoing permissive effects of aldosterone on the permeability responses to vasopressin and theophylline are mediated by a steroid-dependent increase in the accumulation of cAMP in the pertinent epithelial cells, probably as a consequence of a diminution in the rate of degradation of the intracellular nucleotide.

Aldosterone↗
PubMed1969

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

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-(14)C and depress the rate of oxidation of glucose-1-(14)C compared with glucose-6-(14)C. SC-14266 inhibited the effect of dexamethasone on the oxidation of glucose-6-(14)C but did not alter the effect of the steroid on the rate of oxidation of glucose-1-(14)C compared with glucose-6-(14)C, suggesting that the latter is a glucocorticoid effect and the stimulation of glucose-6-(14)C 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.

Aldosterone↗