Hypoxia-augmented constriction of deep femoral artery mediated by inhibition of eNOS in smooth muscle

摘要

In contrast to the conventional belief that systemic arteries dilate under hypoxia, we found that a-adrenergic contraction of rat deep femoral artery (DFA) is largely augmented by hypoxia (HVCdfa) while hypoxia (3% P02) alone had no effect. HVCdfa was consistently observed in both endothelium-intact and -denuded vessels with partial pretone by phenylephrine (PhE) or by other conditions (e.g., K+ channel blocker). Patch-clamp study showed no change in the membrane conductance of DFA myocytes by hypoxia. The RhoA-kinase inhibitor Y27632 attenuated HVCdfa- The nitric oxide synthase inhibitor [nitro-L-arginine methyl ester (l-NAME)] and soluble guan-ylate cyclase inhibitor [oxadiazole quinoxalin (ODQ)] strongly augmented the PhE-pretone, while neither of the agents had effect without pretone.