内源性激肽释放酶-激肽系统在调节蟾蜍膀胱中血管加压素刺激的水流量和尿素通透性方面的作用。
Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.
作者信息
Carvounis C P, Carvounis G, Arbeit L A
出版信息
J Clin Invest. 1981 Jun;67(6):1792-6. doi: 10.1172/jci110219.
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.
摘要
本研究调查了内源性激肽释放酶-激肽系统在蟾蜍膀胱中作为血管加压素作用调节剂的作用。抑肽酶抑制激肽释放酶，导致激肽生成减少，显著增加了血管加压素和8-溴环磷腺苷（8-Br-cAMP）刺激的水流量。激肽酶II抑制剂卡托普利（SQ 14225）增强激肽作用，显著降低血管加压素和8-Br-cAMP刺激的水流量。与水流量相反，抑肽酶降低了血管加压素刺激的尿素通透性，而卡托普利则增加了尿素通透性。我们得出结论，内源性激肽释放酶-激肽系统是血管加压素作用的重要调节剂，它允许对血管加压素刺激的水流量和溶质转运进行单独控制。
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