Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.
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.
D015124:8-Bromo Cyclic Adenosine Monophosphate; D000818:Animals; D001001:Anura; D007611:Aprotinin / Q000494:pharmacology; D001692:Biological Transport / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D002463:Cell Membrane Permeability; D000242:Cyclic AMP / Q000031:analogs & derivatives / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007610:Kallikreins / Q000378:metabolism*; D007705:Kinins / Q000378:metabolism*; D014508:Urea / Q000378:metabolism*; D001743:Urinary Bladder / Q000187:drug effects* / Q000201:enzymology; D014667:Vasopressins / Q000494:pharmacology*; D014867:Water / Q000378:metabolism*
D007705:Kinins; D014867:Water; D014667:Vasopressins; D015124:8-Bromo Cyclic Adenosine Monophosphate; D014508:Urea; D007611:Aprotinin; D002216:Captopril; D000242:Cyclic AMP; D007610:Kallikreins