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Am J Physiol 206: 136-142, 1964;
0002-9513/64 $5.00
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Effects of hormones on Na and H2O transport and on phospholipid metabolism in toad bladder

Sarah Hestrin-Lerner 1 and Lowell E. Hokin 1

1 Department of Physiological Chemistry, University of Wisconsin, Madison, Wisconsin

Incubation of tied paired lobes of bladder from Bufo marinus with 0.025–0.25 U/ml of oxytocin led to appreciable stimulations of both sodium transport and of water transport from the mucosal (luminal) to serosal side. Incubation with aldosterone led to a very slight stimulation of sodium transport, which was statistically significant, in one out of three series. P32 from orthophosphate was incorporated into phosphatidic acid, phosphatidyl ethanolamine, phosphatidyl choline, and phosphatidyl inositol. There were no statistically significant stimulations in the incorporation of P32 into phosphatidic acid, phosphatidyl choline, or phosphatidyl inositol at any concentration of oxytocin. However, there was a statistically significant stimulation of P32 incorporation into phosphatidyl ethanolamine with 0.025 U/ml oxytocin. There was a statistically significant inhibition in incorporation in phosphatidyl choline and phosphatidyl inositol with 0.25 U/ml oxytocin. Cholinergic agents did not produce statistically significant stimulations of either water or sodium transport in toad or turtle bladders, but they led to significant stimulations of incorporation of P32 into some of the phosphatides (phosphatidic acid, phosphatidyl choline, and phosphatidyl inositol in the toad bladder, and phosphatidic acid and phosphatidyl inositol in turtle bladder). On the basis of the fine structure of the epithelium of the toad bladder it is suggested that the phospholipid effect in response to cholinergic agents may be related to stimulation of the secretion of an organic material by the epithelial and/or goblet cells.

Key Words: phospholipids and sodium transport • phosphatidic acid phosphatidyl inositol • vasopressin • acetyl-ßbeta;-methyl-choline

Submitted on May 1, 1963







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Copyright © 1964 by the American Physiological Society.