HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/6/H2454    most recent 00364.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Sun, D. Articles by Kaley, G. Search for Related Content PubMed PubMed Citation Articles by Sun, D. Articles by Kaley, G.

Mechanical compression elicits NO-dependent increases in coronary flow

Department of Physiology, New York Medical College, Valhalla, New York 10595

Submitted 15 April 2004 ; accepted in final form 9 August 2004

Our previous studies have 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 extracardiac compression. To minimize the impact of metabolic vasodilatation and rhythmic changes in shear stress, nonbeating hearts, by perfusing the hearts with a solution containing 20 mM KCl, were used. After extracardiac compression for 10 or 20 s, coronary flow increased significantly, concurrent with an increased release of nitrite into the coronary effluent and increased phosphorylation of endothelial NO synthase 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, the release of vascular compression elicited a NO-dependent dilation. Thus this study reveals a new mechanism that, via coronary vascular deformation, elicited by cardiac contraction, stimulates the endothelium to release NO, leading to increased coronary perfusion.

endothelial deformation; nitric oxide; coronary circulation

This article has been cited by other articles:

				T. R. Uhrenholt, J. Schjerning, P. M. Vanhoutte, B. L. Jensen, and O. Skott Intercellular calcium signaling and nitric oxide feedback during constriction of rabbit renal afferent arterioles Am J Physiol Renal Physiol, April 1, 2007; 292(4): F1124 - F1131. [Abstract] [Full Text] [PDF]

				N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev, October 1, 2006; 86(4): 1263 - 1308. [Abstract] [Full Text] [PDF]

				P. S. Clifford, H. A. Kluess, J. J. Hamann, J. B. Buckwalter, and J. L. Jasperse Mechanical compression elicits vasodilatation in rat skeletal muscle feed arteries J. Physiol., April 15, 2006; 572(2): 561 - 567. [Abstract] [Full Text] [PDF]

				M. Azzawi and C. Austin Extravascular pressure modulates responses of isolated rat coronary arteries to vasodilator, but not vasoconstrictor, stimuli Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H1151 - H1156. [Abstract] [Full Text] [PDF]