Printed i U.S.A. Verapamil Inhibition of Vasopressin-Stimulated Water Flow: Possible Role of Intracellular Calcium1

The effects of the organic calcium antagonists verapamil and verapamil to the bathing media dunng recovery from a vasopres-methoxyverapamil (D-600) on vasopressin-stimulated water flow sin stimulus to block reuptake of calcium into the epitheliaJ cells in response to an osmotic gradient were investigated. When inhibited water flow in response to a subsequent incubation with toad bladders were exposed to either verapamil or D-600 for 60 vasopressin to a greater extent than the inhibition of water flow mm, vasopressin-stimulated water flow was inhibited. In the when verapamil was present only before exposure to vasopres-presence of verapamil (1 00 SM), water flow decreased from 38 sin. Inhibition was also greater in the presence of lower extra-± 3 to 26 ± 3 mg/min/hemibladder (P <.05, n = 5) and in the cellular calcium concentrations. The results are consistent with presence of D-600 (1 00 zM) from 48 ± 3 to 32 ± 4 mg/min / the notion that the calcium antagonists inhibit vasopressin-stim-hemibladder (P <.02, n = 5). When preincubated with hemiblad- ulated water flow by virtue of depleting a Critical pool of intracel-ders for 90 mm they also inhibited basal 45Ca uptake into isolated lular calcium rather than preventing the simultaneous entry of toad bladder epithelial cells (from 1.58 ± 0.20 to 1.02 ± 0.1 4 calcium from extracellular sites during the exposure to vasopres-nmol/mg of protein per 5 mm, P <.05, n = 6). Addition of sin