Cellular and membrane events involved in the K-induced increase in water permeability of toad skin.

Exposure of the inner surface of toad skin (Bufo marinus) to high [K+] resulted in a marked (up to 7-fold) increase in water permeability (Pf) that was more marked in KC1-Ringer than in K2SO4-Ringer. Although high [K+] did not elicit a maximal increase in Pf, it blunted the hydrosmotic responses to vasopressin, isoproterenol and cAMP. Both "post-cAMP" inhibitors of stimulated water flow, such as diamide and vanadate, and "pre-cAMP" inhibitors, such as methohexital and propranolol, markedly reduced the K response, while exposure to Ca2+-free, KC1-Ringer did not inhibit water flow. Intramembrane particle aggregates, similar to those induced by cAMP-mediated hydrosmotic agents, were seen in the apical membrane of granular cells, just beneath the stratum corneum, in skins exposed to KC1. Available evidence indicates that cAMP might mediate, at least partially, the hydrosmotic effect of high [K+]. In contrast, a role of voltage-dependent Ca2+ channels, described in other cell systems depolarized with K, was not apparent in toad skin.