Reoxygenation-Induced Relaxation of Coronary Arteries A Novel Endothelium-Dependent Mechanism

Abstract Coronary artery contractility is well known to be modulated by oxygen partial pressure. Both smooth muscle and the endothelium contribute to coronary artery oxygen sensitivity. Mechanisms underlying endothelium-dependent effects of oxygen include the sensitivity of the nitric oxide/en-dothelium-derived relaxing factor (EDRF), hydrogen perox-ide, and eicosanoid pathways. In the present study, we char-acterize a novel endothelium-dependent component of porcine coronary artery oxygen sensitivity that is independent of these known pathways. Porcine coronary arteries were stimulated with either KCI or U46619. Hypoxia elicited a transient increase in force that was much greater in endothe-lium-intact arteries. This effect was abolished by nitric oxide/ EDRF pathway inhibitors N0-monomethyl-L-arginine and N-nitro-L-arginine. In the steady state, hypoxia reduced iso