Heavy metal-induced alterations in ion transport by turtle urinary bladder.

Previous studies of heavy metal salt-induced acute renal failure demonstrated abnormalities of fluid and solute transport by nephron segments and alterations in glomerular filtration rate and renal hemodynamics. To determine the direct effects of uranyl nitrate (UN) or HgCl2 on ion transport, their effects were studied on the isolated urinary bladder of the turtle. Unidirectional 24Na+ and 36Cl- fluxes were measured across short-circuited bladders. The addition of 0.1 mM UN to the mucosal solution resulted in a 69.9 +/- 4% (SEM) decrease in short-circuit current (SCC) without change in transepithelial resistance. Net Na+ flux (7.95 +/- 0.81 mueq/h per 8 cm2) decreased by the same magnitude as the SCC, primarily due to a 5.75 +/- 0.76 mueq/h per 8 cm2 decrease in the mucosal- (M) to-serosal (S) Na+ flux. Net Cl- flux decreased also primarily due to a decrease in M-to-S Cl- flux. Addition of 0.4 mM UN to S did not measurably affect the SCC or ion fluxes. The addition of 10 muM HgCl2 in another group of bladders reduced SCC and M-to-S Na+ flux by 81 +/- 7% without change in Cl- fluxes or resistance. The removal of either UN or HgCl2 from M by washing did not reverse the decreased SCC, but after washing addition of either dithiothreitol, 2 mM, or amphotericin B, 20 mug/ml, to M completely reversed the effects of UN or HgCl2 on SCC. These studies suggest that heavy metal salts inhibit Na+ transport by the turtle bladder without altering passive ion fluxes.