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Circulation Research. 1996;79:840-848

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*Compound via MeSH
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*NITRIC OXIDE
(Circulation Research. 1996;79:840-848.)
© 1996 American Heart Association, Inc.


Articles

Function and Production of Nitric Oxide in the Coronary Circulation of the Conscious Dog During Exercise

Robert D. Bernstein, Francisca Y. Ochoa, Xaobin Xu, Paul Forfia, Weiqun Shen, Carl I. Thompson, Thomas H. Hintze

the Department of Physiology, New York Medical College, Valhalla.

Correspondence to Thomas H. Hintze, PhD, Professor, Department of Physiology, New York Medical College, Valhalla, NY 10595.

This study determined the changes in NO production from the coronary circulation of the conscious dog during exercise. The role of endogenous NO as it relates to coronary flow, myocardial work, and metabolism was also studied. Mongrel dogs were chronically instrumented for measurements of coronary blood flow (CBF), ventricular and aortic pressures, and ventricular diameter, with catheters in the aorta and coronary sinus. Acute exercise (5 minutes at 3.6, 5.9, and 9.1 mph) was performed, and hemodynamic measurements and blood samples were taken at each exercise level. Nitro-L-arginine (NLA, 35 mg/kg IV) was given to block NO synthesis, and the exercise was repeated. Blood samples were analyzed for oxygen, plasma nitrate/nitrite (an index of NO), lactate, glucose, and free fatty acid (FFA) levels. Acute exercise caused significant elevations in NO production by the coronary circulation (46±23, 129±44, and 63±32 nmol/min at each speed respectively, P<.05). After NLA, there was no measurable NO production at rest or during exercise. Blockade of NO synthesis resulted in elevations in myocardial oxygen consumption and reductions in myocardial FFA consumption for comparable levels of CBF and cardiac work. The metabolic changes after NLA occurred in the absence of alterations in myocardial lactate or glucose consumptions. NO production by the coronary circulation is increased with exercise and blocked by NLA. The absence of NO in the coronary circulation during exercise does not affect levels of CBF, because it shifts the relationship between cardiac work and myocardial oxygen consumption, suggesting that endogenous NO modulates myocardial metabolism.


Key Words: nitric oxide • endothelium-derived relaxing factor • coronary resistance • myocardial metabolism • oxygen consumption




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Am. J. Physiol. Heart Circ. Physiol.Home page
P. R. Forfia, X. Zhang, D. R. Knight, A. H. Smith, C. P. A. Doe, E. A. Wolfgang, D. M. Flynn, M. S. Wolin, and T. H. Hintze
NO modulates myocardial O2 consumption in the nonhuman primate: an additional mechanism of action of amlodipine
Am J Physiol Heart Circ Physiol, June 1, 1999; 276(6): H2069 - H2075.
[Abstract] [Full Text] [PDF]


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Circ. Res.Home page
K. E. Loke, P. I. McConnell, J. M. Tuzman, E. G. Shesely, C. J. Smith, C. J. Stackpole, C. I. Thompson, G. Kaley, M. S. Wolin, and T. H. Hintze
Endogenous Endothelial Nitric Oxide Synthase–Derived Nitric Oxide Is a Physiological Regulator of Myocardial Oxygen Consumption
Circ. Res., April 16, 1999; 84(7): 840 - 845.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
D. J. Duncker, J. H. Traverse, Y. Ishibashi, and R. J. Bache
Effect of NO on transmural distribution of blood flow in hypertrophied left ventricle during exercise
Am J Physiol Heart Circ Physiol, April 1, 1999; 276(4): H1305 - H1312.
[Abstract] [Full Text] [PDF]


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Cardiovasc ResHome page
G. J Crystal and X. Zhou
Nitric oxide does not modulate the increases in blood flow, O2 consumption, or contractility during CaCl2 administration in canine hearts
Cardiovasc Res, April 1, 1999; 42(1): 232 - 239.
[Abstract] [Full Text] [PDF]


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Circ. Res.Home page
F. A. Recchia, P. I. McConnell, R. D. Bernstein, T. R. Vogel, X. Xu, and T. H. Hintze
Reduced Nitric Oxide Production and Altered Myocardial Metabolism During the Decompensation of Pacing-Induced Heart Failure in the Conscious Dog
Circ. Res., November 16, 1998; 83(10): 969 - 979.
[Abstract] [Full Text] [PDF]


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Circ. Res.Home page
S. K. Laycock, T. Vogel, P. R. Forfia, J. Tuzman, X. Xu, M. Ochoa, C. I. Thompson, A. Nasjletti, and T. H. Hintze
Role of Nitric Oxide in the Control of Renal Oxygen Consumption and the Regulation of Chemical Work in the Kidney
Circ. Res., June 29, 1998; 82(12): 1263 - 1271.
[Abstract] [Full Text] [PDF]


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Circ. Res.Home page
Y.-W. Xie, P. M. Kaminski, and M. S. Wolin
Inhibition of Rat Cardiac Muscle Contraction and Mitochondrial Respiration by Endogenous Peroxynitrite Formation During Posthypoxic Reoxygenation
Circ. Res., May 4, 1998; 82(8): 891 - 897.
[Abstract] [Full Text] [PDF]


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Circ. Res.Home page
Y. Ishibashi, D. J. Duncker, J. Zhang, and R. J. Bache
ATP-Sensitive K+ Channels, Adenosine, and Nitric Oxide–Mediated Mechanisms Account for Coronary Vasodilation During Exercise
Circ. Res., February 23, 1998; 82(3): 346 - 359.
[Abstract] [Full Text] [PDF]


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J. Appl. Physiol.Home page
J. L. Parker, M. L. Mattox, and M. H. Laughlin
Contractile responsiveness of coronary arteries from exercise-trained rats
J Appl Physiol, August 1, 1997; 83(2): 434 - 443.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
S. Setty, J. D. Tune, and H. F. Downey
Nitric oxide modulates right ventricular flow and oxygen consumption during norepinephrine infusion
Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H696 - H703.
[Abstract] [Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
M. Takamura, R. Parent, and M. Lavallee
Enhanced contribution of NO to exercise-induced coronary responses after alpha -adrenergic receptor blockade
Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H508 - H515.
[Abstract] [Full Text] [PDF]