Ca2+ entry through the apical membrane reduces antidiuretic hormone-induced hydroosmotic response in toad urinary bladder.

The role of Ca2+ in the regulation of antidiuretic hormone(ADH)-induced water permeability of the apical membrane of the toad urinary bladder was examined. The effects of modifying Ca2+ entry through the apical membrane of toad urinary bladders on the hydroosmotic water flow (phi H2O) and short circuit current (Isc) were measured. In most experiments the bladders were treated with small amounts of Ag+ (10(-7) mol/l) on the apical side. This treatment was used because previous experiments indicate that it markedly increases alkali-earth cation fluxes through an amiloride-insensitive cation channel in the apical membrane of the urinary bladder. Moreover, when Ca2+ is the major cation in the apical solution of these Ag(+)-treated bladders, Isc is mostly due to Ca2+ entry through the apical membrane. Ag+ increased Isc and simultaneously inhibited phi H2O in bladders perfused with Ca2+ solutions on the apical side. Addition of La3+ to the apical solution reversed the stimulation of Isc and the inhibition of phi H2O produced by Ag+. When bladders were perfused with Ca2(+)-free solutions on the apical side, addition of Ag+ did not inhibit phi H2O while the stimulation of cation movements through the amiloride-insensitive cation channel persisted. In bladders perfused with apical Ca2+ solutions and treated with chlorophenyl thio-cyclic adenosine monophosphate (ClPheS-cAMP) the addition of Ag+ did not inhibit phi H2O while it still increased Isc. Finally, addition of Ca2+ to the apical solution of bladders not treated with Ag+ reduced phi H2O.(ABSTRACT TRUNCATED AT 250 WORDS)