Water flow in the toad urinary bladder in response to vasopressin: role of potassium.

In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10(-5) M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.