Prostacyclin as a hyperpolarizing and a vasoconstricting factor. Upper panel: In the guinea pig isolated carotid artery, prostacyclin (PGI2) and its stable analogue, iloprost, produce vascular smooth muscle hyperpolarization. The KATP blocker, glibenclamide (1 μM), inhibits these hyperpolarizations. In the presence of glibenclamide, prostacyclin, but not iloprost, produces a rhythmic electrical activity, which is inhibited by the TP receptor antagonist Bay U3405. The concentration-dependent hyperpolarization produced by prostacyclin, but not that to iloprost, is significantly potentiated by the presence of Bay U3405. Lower panel: In rat quiescent isolated aortic rings and in the presence of the NO-synthase inhibitor, L-nitro-arginine (100 μM), prostacyclin produces concentration-dependent contractions. These contractions are blocked by the TP receptor antagonist, S 18886, and are revealed following either NO-synthase blockade or endothelial denudation.

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From: Chapter 4, Endothelium-Dependent Regulation of Vascular Tone

Cover of The Endothelium
The Endothelium: Part 1: Multiple Functions of the Endothelial Cells—Focus on Endothelium-Derived Vasoactive Mediators.
Félétou M.
San Rafael (CA): Morgan & Claypool Life Sciences; 2011.
Copyright © 2011 by Morgan & Claypool Life Sciences Publishers.

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