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Rapid Publication Free access | 10.1172/JCI110219

Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.

C P Carvounis, G Carvounis, and L A Arbeit

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Published June 1, 1981 - More info

Published in Volume 67, Issue 6 on June 1, 1981
J Clin Invest. 1981;67(6):1792–1796. https://doi.org/10.1172/JCI110219.
© 1981 The American Society for Clinical Investigation
Published June 1, 1981 - Version history
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Abstract

This study investigates the endogenous kallikrein-kinin system's role as a modulator of vasopressin action in the toad urinary bladder. Kalli-krein inhibition by aprotinin, which results in decreased kinin production, significantly increased both vasopressin and 8-Br-cyclic (c) AMP-stimulated water flow. Kinin potentiation by the kininase II inhibitor captopril (SQ 14225) significantly decreased vasopressin and 8-Br-cAMP-stimulated water flow. In contrast to water flow, vasopressin-stimulated urea permeability was decreased by aprotinin and increased by captopril. We conclude that the endogenous kallikrein-kinin system represents a significant modulator of vasopressin action and it permits separate control of vasopressin-stimulated water flow and solute transport.

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