Calcium Inhibition of the Action of Vasopressin on the Urinary Bladder of the Toad*

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Abstract
At low concentrations of vasopressin (1 mU per ml) a rise in the Ca++ concentration from 2.7 to 10 moles per L depressed the hormonally induced increase in the flow of water at a fixed osmotic gradient by 65%. The Ca++ effect was completely reversed by increasing the vasopressin concentration to 66 mU per ml. A rise in Ca++ concentration to 10 mmoles per L also depressed the vasopressin-mediated increase in the urea permeability coefficient by 45% at low concentrations of vasopressin (1 mU per ml). In the presence of high concentrations of vasopressin (100 mU per ml), a rise in Ca++ concentration to 10 mmoles per L produced a lesser depression in the hormonal effect on urea diffusion that was not statistically significant. In contrast to the effects on water and urea, raising the concentration of Ca++ had no influence on the action of vasopressin on active Na+ transport. The ability of Ca++ to dissociate the effects of vasopressin on water and urea from the effect on Na+ transport implies a divergence in the action of the hormone that requires a modification of the unitary hypothesis. Two alternative possible explanations have been presented, taking into account the absence of an effect of Ca++ on the action of adenosine-3[image],5[image]-monophosphate (cyclic AMP) on osmotic flow of water.