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* Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, Texas 76107;
Division of Cardiovascular Biology, Shen Nippon Biomedical Laboratories, Ltd., USA, Redmond, Washington 98052; and
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195
Under normal physiological conditions, coronary blood flow is closely matched with the rate of myocardial oxygen consumption. This matching of flow and metabolism is physiologically important due to the limited oxygen extraction reserve of the heart. Thus, when myocardial oxygen consumption is increased, as during exercise, coronary vasodilation and increased oxygen delivery are critical to preventing myocardial underperfusion and ischemia. Exercise coronary vasodilation is thought to be mediated primarily by the production of local metabolic vasodilators released from cardiomyocytes secondary to an increase in myocardial oxygen consumption. However, despite various investigations into this mechanism, the mediator(s) of metabolic coronary vasodilation remain unknown. As will be seen in this review, the adenosine, K+ATP channel and nitric oxide hypotheses have been found to be inadequate, either alone or in combination as multiple redundant compensatory mechanisms. Prostaglandins and potassium are also not important in steady-state coronary flow regulation. Other factors such as ATP and endothelium-derived hyperpolarizing factors have been proposed as potential local metabolic factors, but have not been examined during exercise coronary vasodilation. In contrast, norepinephrine released from sympathetic nerve endings mediates a feed-forward ßadrenoceptor coronary vasodilation that accounts for 
25% of coronary vasodilation observed during exercise. There is also a feed-forward 
-adrenoceptor-mediated vasoconstriction that helps maintain blood flow to the vulnerable subendocardium when heart rate, myocardial contractility, and oxygen consumption are elevated during exercise. Control of coronary blood flow during pathophysiological conditions such as hypertension, diabetes mellitus, and heart failure is also addressed.
Key Words: adenosine • nitric oxide • K+ATP channels • ß-feed-forward vasodilation • -adrenoceptor vasoconstriction
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