Ca2+ entry through the apical membrane reduces antidiuretic hormone-induced hydroosmotic response in toad urinary bladder |
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Authors: | Willy Van Driessche David Erlij Isabelle Aelvoet |
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Institution: | (1) Laboratory of Physiology, KU Leuven, Campus Gasthuisberg, B-3000 Leuven, Belgium;(2) Department of Physiology, SUNY Health Science Center Brooklyn, 450 Clarkson Avenue, 11203 Brooklyn, NY, USA |
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Abstract: | 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 H2O) and short circuit current (I
sc) 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, I
sc is mostly due to Ca2+ entry through the apical membrane. Ag+ increased I
sc and simultaneously inhibited H2O in bladders perfused with Ca2+ solutions on the apical side. Addition of La3+ to the apical solution reversed the stimulation of I
sc and the inhibition of H2O produced by Ag+. When bladders were perfused with Ca2+-free solutions on the apical side, addition of Ag+ did not inhibit 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 H2O while it still increased I
sc. Finally, addition of Ca2+ to the apical solution of bladders not treated with Ag+ reduced H2O. These results taken together with other findings in the literature suggest: (1) Ca2+ entry through the Ag+-treated amiloride-insensitive cation channel of the apical membrane inhibits H2O; (2) the effects of Ca2+ entry are at a regulatory site that precedes the interaction of cAMP with the water channels; (3) it is also possible that Ca2+ entry through the unmodified amiloride-insensitive cation channel may have some inhibitory effect on H2O. |
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Keywords: | Water transport Antidiuretic hormone Oxytocin Cyclic adenosine monophosphate |
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