Abstract

Unidirectional 32P-phosphate and 3H-mannitol fluxes were simultaneously measured, at two minutes intervals, in frog urinary bladders. The spontaneous or externally imposed transepithelial potential (PD) and short circuit current (SCC) were also recorded in most experiments. It was observed that: (1) Phosphate transfer was rapidly and reversibly modified by changes in mucosal sodium concentration in open circuit conditions. (2) Between four and six minutes after changing mucosal NaCl concentration, phosphate fluxes reached a new steady-state value. (3) The observed correlation between the Na-dependent phosphate flux and the Na-dependent transmembrane potential was high (r = 0.99, N = 12). (4) In open circuit conditions, the mucosa-to-serosa unidirectional phosphate fluxes were inhibited by 10(-5) M amiloride, while the serosa-to-mucosa movements were increased. (5) On the contrary, no effects of mucosal NaCl concentration or amiloride on the mucosa-to-serosa phosphate fluxes were detected in short circuit conditions. (6) The transepithelial phosphate transfer was linearly related to phosphate concentration and insensitive to arsenate (10(-3) M) action. (7) An externally imposed PD was less effective for driving a phosphate movement than the one depending on Na, suggesting some type of coupling between Na+ and phosphate transports. (8) The mucosa-to-serosa phosphate fluxes were reduced by parathyroid hormone and oxytocin. Maximum inhibition was observed four minutes after the hormonal action. It is concluded that the transepithelial PD plays a major role in phosphate handling in frog urinary bladder.

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