ANION TRANSPORT INHIBITORS - EFFECTS ON WATER AND SODIUM-TRANSPORT IN THE TOAD URINARY-BLADDER

Acidification of the medium bathing the serosal surface of the toad urinary bladder results in impairment of the water permeability response to vasopressin. The magnitude of the hydrosmotic response to a maximal concentration of either vasopressin or the cyclic nucleotide analog 8-(p-chlorophenythio)-cAMP (ClPhS-cAMP) was progressively reduced when serosal bath pH was decreased from 8.5-6.5. The disulfonic stilbenes SITS and DIDS and the diuretic furosemide, agents known to interfere with anion transport and with the regulation of intracellular pH in other tissues, inhibited the water flow responses to vasopressin and C1PhS-cAMP in a pH-dependent manner when added to the serosal bathing medium. Inhibition of the hydrosmotic response to 10-5 M C1PS-cAMP was estimated to be half-maximal at 1.5 .times. 10-4 M SITS, 2 .times. 105 M DIDS and 1 .times. 10-5M furosemide. The degree of inhibition induced by the anion transport inhibitors varied inversely with the concentration of exogenous cyclic nucleotide. SITS[4-acetamido-4''-isothiocyanostilbene-2-2''-disulfonic acid], DIDS [4,4''-diisocyano-2,2''disulfonic acid stilbene] and furosemide had no effect on either basal or vasopressin-stimulated short-circuit current at serosal pH 8.5; all 3 agents inhibited basal short-circuit current at pH 7.1 but had no effect on the natriferic response to vasopressin. Apparently changes in intracellualar H ion and/or anion concentration can selectively inhibit the increase in water permeability elicited by vasopressin at a step(s) distal to the generation of cAMP.