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Am J Physiol Heart Circ Physiol 282: H1296-H1303, 2002. First published November 15, 2001; doi:10.1152/ajpheart.00179.2001
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Vol. 282, Issue 4, H1296-H1303, April 2002

Role of myocardium and endothelium in coronary vascular smooth muscle responses to hypoxia

Cornel J. M. Kerkhof, Peter J. W. Van Der Linden, and Pieter Sipkema

Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, Amsterdam 1081 BT, The Netherlands

Hypoxia triggers a mechanism that induces vasodilation in the whole heart but not necessarily in isolated coronary arteries. We therefore studied the role of cardiomyocytes (CM), smooth muscle cells (SMC), and endothelial cells (EC) in coronary responses to hypoxia (PO2 of 5-10 mmHg). In an attempt to determine the factor(s) released in response to hypoxia, we inhibited the contribution of adenosine, ATP-sensitive K+ channels, prostaglandins, and nitric oxide. Isolated rat septal artery segments without (-T) and with a layer of cardiac tissue (+T) were mounted in a double wire myograph, and constriction was induced. Hypoxia induced a decrease in isometric force of 21% and 61% in -T and +T segments, respectively (P < 0.05). EC removal increased the relaxation to hypoxia in -T segments to 33% but had the same effect in +T segments (61%). Only one of the inhibitors, the adenosine antagonist in +T segments, partially affected the relaxation due to hypoxia. The role of adenosine is thus limited and other mechanisms have to contribute. We conclude that hypoxia induces a relaxation of SMC that is augmented by the presence of CM and blunted by the endothelium. A single mediator does not induce those effects.

endothelial cells; smooth muscle cells; cardiomyocytes; ATP-sensitive potassium channels; adenosine


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