© 1999 American Heart Association, Inc.
Cellular Biology |
Self-Protection by Cardiac Myocytes Against Hypoxia and Hyperoxia
From the Department of Physiology (S.W.), School of Medicine, University of Pennsylvania, Philadelphia, Pa, and INSERM Unit 127 (L.R., J.L.S.), IFR Circulation, Université D. Diderot, and INSERM Unit 141 (D.H.), Hôpital Lariboisière, Paris, France.
Correspondence to Saul Winegrad, Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6085. E-mail bsg{at}mail.med.upenn.edu
Abstract—Cardiac muscle must
maintain a continuous balance between its energy supply and work
performed. An important mechanism involved in achievement of this
balance is cross talk via chemical signals between cardiac myocytes and
the cardiac muscle vascular system . This has been demonstrated by
incubating isolated cardiac myocytes in different concentrations of
oxygen and then assaying the conditioned media for vasoactive
substances on isolated aortic rings and small-resistance arteries. With
increasing oxygen concentrations above 6%, cardiac myocytes produce
increasing amounts of angiotensin I, which is converted to
angiotensin II by the blood vessel. The
angiotensin II stimulates vascular
endothelial cells to secrete endothelin and increase
vascular tone. Below 6% oxygen, cardiac myocytes secrete
adenosine, which acts directly on vascular smooth muscle to
block the effect of 
-adrenergic agonists and reduce vascular tone.
In an intact heart, the net effect of these 2 regulatory systems would
be the maintenance of oxygen concentration within a narrow
range at the cardiac myocytes. By acting as oxygen sensors, cardiac
myocytes modulate vascular tone according to the needs of the myocytes
and reduce potential problems of hypoxia and extensive
formation of reactive oxygen species.
Key Words: adenosine • angiotensin • cardiac myocyte • endothelin • regulation of blood flow
This article has been cited by other articles:
 |
|
 |
|
  O. Yamaguchi, T. Kaneshiro, S.-i. Saitoh, T. Ishibashi, Y. Maruyama, and Y. Takeishi Regulation of coronary vascular tone via redox modulation in the {alpha}1-adrenergic-angiotensin-endothelin axis of the myocardium Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H226 - H232. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. H. McNulty, B. J. Robertson, M. A. Tulli, J. Hess, L. A. Harach, S. Scott, and L. I. Sinoway Effect of hyperoxia and vitamin C on coronary blood flow in patients with ischemic heart disease J Appl Physiol, May 1, 2007; 102(5): 2040 - 2045. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Thomson, G. B. Drummond, W. S. Waring, D. J. Webb, and S. R. J. Maxwell Effects of short-term isocapnic hyperoxia and hypoxia on cardiovascular function J Appl Physiol, September 1, 2006; 101(3): 809 - 816. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. K. Sen, S. Khanna, and S. Roy Perceived hyperoxia: Oxygen-induced remodeling of the reoxygenated heart Cardiovasc Res, July 15, 2006; 71(2): 280 - 288. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Takahashi, T. Komaru, S. Takeda, K. Sato, H. Kanatsuka, and K. Shirato Nitric oxide inhibition unmasks ischemic myocardium-derived vasoconstrictor signals activating endothelin type A receptor of coronary microvessels Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H85 - H91. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Merkus, A. K. Brzezinska, C. Zhang, S. Saito, and W. M. Chilian Cardiac myocytes control release of endothelin-1 in coronary vasculature Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2088 - H2092. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. H. McNulty, N. King, S. Scott, G. Hartman, J. McCann, M. Kozak, C. E. Chambers, L. M. Demers, and L. I. Sinoway Effects of supplemental oxygen administration on coronary blood flow in patients undergoing cardiac catheterization Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1057 - H1062. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Govindaraju, H. Teoh, Q. Hamid, P. Cernacek, and M. E. Ward Interaction between endothelial heme oxygenase-2 and endothelin-1 in altered aortic reactivity after hypoxia in rats Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H962 - H970. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Roy, S. Khanna, W. A. Wallace, J. Lappalainen, C. Rink, A. J. Cardounel, J. L. Zweier, and C. K. Sen Characterization of Perceived Hyperoxia in Isolated Primary Cardiac Fibroblasts and in the Reoxygenated Heart J. Biol. Chem., November 21, 2003; 278(47): 47129 - 47135. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Roy, S. Khanna, A. A. Bickerstaff, S. V. Subramanian, M. Atalay, M. Bierl, S. Pendyala, D. Levy, N. Sharma, M. Venojarvi, et al. Oxygen Sensing by Primary Cardiac Fibroblasts: A Key Role of p21Waf1/Cip1/Sdi1 Circ. Res., February 21, 2003; 92(3): 264 - 271. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Merkus, D. J. Duncker, and W. M. Chilian Metabolic regulation of coronary vascular tone: role of endothelin-1 Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H1915 - H1921. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Mak, E. R. Azevedo, P. P. Liu, and G. E. Newton Effect of Hyperoxia on Left Ventricular Function and Filling Pressures in Patients With and Without Congestive Heart Failure Chest, August 1, 2001; 120(2): 467 - 473. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Boemke, B. Hocher, N. Schleyer, M. O. Krebs, and G. Kaczmarczyk Hemodynamic, renal, and endocrine responses to acute ETA blockade at different ANG II plasma levels Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2001; 280(5): R1322 - R1331. [Abstract] [Full Text] [PDF]
|
|