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1 Physiology, New York Medical College, Valhalla, NY, USA
* To whom correspondence should be addressed. E-mail: dong_sun{at}nymc.edu.
Our previous studies demonstrated that a decrease in arteriolar diameter that causes endothelial deformation elicits the release of nitric oxide (NO). Thus, we hypothesized that cardiac contraction, via deformation of coronary vessels, elicits the release of NO and increases in coronary flow. Coronary flow was measured at a constant perfusion pressure of 80 mmHg in Langendorff preparations of rat hearts. Hearts were placed in a sealed chamber surrounded with perfusion solution. The chamber pressure could be increased from 0 to 80 mmHg to generate extra-cardiac compression. To minimize the impact of metabolic vasodilatation and rhythmic changes in shear stress, non-beating hearts, by perfusing the hearts with a solution containing 20 mM of KCl, were used. After extra-cardiac compression for 10 or 20 seconds, coronary flow increased significantly, concurrent with an increased release of nitrite into the coronary effluent and increased phosphorylation of eNOS in the hearts. Inhibition of NO synthesis eliminated the compression-induced increases in coronary flow. Shear stress-induced dilation could not account for this increased coronary flow. Furthermore, in isolated coronary arterioles, without intraluminal flow, release of vascular compression elicited a NO-dependent dilation. Thus, this study reveals a new mechanism which via coronary vascular deformation, elicited by cardiac contraction, stimulates the endothelium to release NO, leading to increased coronary perfusion.
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