High [K+] alters the stimulus-hydrosmotic response coupling in toad bladder.

Substitution of K+ for Na+ in the Ringer solution bathing the inner surface of toad urinary bladders (Bufo marinus) had no effect on basal water permeability but significantly altered the stimulus-hydrosmotic response of this epithelium. In chloride-Ringer, high [K+] increased the hydrosmotic responses to submaximal stimulations induced by vasopressin or exogenous cAMP, while the responses to theophylline or serosal hypertonicity were decreased. In sulfate-Ringer, all these responses were enhanced but for that induced by serosal hypertonicity which was actually diminished. As a step towards determining if Ca2+ might mediate the K+-induced effects on water flow, experiments were conducted either in the presence of a Ca2+ "antagonist" (cobalt) or in nominally Ca2+-free Ringer. In both conditions the hydrosmotic effects of vasopressin and cAMP were markedly reduced. The results raise the possibility that a transient Ca2+ influx through voltage-sensitive, Co2+-blockade Ca2+ channels may play a role in the stimulus-hydrosmotic response of toad urinary bladder.