alpha-Adrenoceptor attenuation of the coronary vascular response to severe exercise in the conscious dog.

The hypothesis that a-adrenergic vasoconstriction could limit the extent of coronary vasodilation during spontaneous strenuous exercise was tested in normal mongrel dogs instrumented for the measurement of left circumflex coronary blood flow, aortic pressure, and left ventricular pressure.These signals were radiotelemetered at rest and during free-ranging exercise with dogs either in the unblocked condition, or after ^-receptor blockade (propranolol, 1 mg/kg), a-receptor blockade (phentolamine, 1-2 mg/kg), or combined ft-and a-receptor blockades.Heart rate was held constant by electrical stimulation throughout the exercise period.After a-receptor blockade alone, late diastolic coronary resistance decreased during exercise to a significantly lower (P < 0.01) level (0.36 ± 0.06 mm Hg/ml per min) than in the unblocked condition (0.52 ± 0.04 mm Hg/ml per min).In the presence of /9-adrenergic blockade, exercise induced insignificant increases in mean left circumflex coronary blood flow and decreases in late diastolic coronary resistance.In contrast, after pretreatment causing combined a and p blockade, both the increase (P < 0.05) in mean left circumflex coronary blood flow (22 ± 4 ml/min) and the decrease (P < 0.01) in late diastolic coronary resistance (0.35 ± 0.07 mm Hg/ml per min) during exercise were significantly greater.This enhanced coronary vascular dilation during exercise following a-receptor blockade could not be attributed to increased metabolically induced vasodilation secondary to changes in aortic pressure, heart rate, left ventricular systolic pressure, or left ventricular dP/dt.These observations strongly support the hypothesis that a receptors in the coronary circulation can act to attenuate alterations in coronary vascular resistance, even during periods of high sympathetic discharge, as occurs during severe exercise.Ore Res 45: 884-660, 1979BECAUSE of the striking ability of the heart to match an increase in metabolic demand with an increase in nutrient supply, it has been presumed that control of the coronary circulation is primarily an intrinsic phenomenon involving the release of vasoactive metabolites from myocardial cells (Berne, 1964).In recent years, however, work by a number of investigators supports the concept that the coronary circulation is also under direct neural control.For instance, it has become increasingly apparent that sympathetic activation can result in a-adrenergic-mediated coronary vasoconstriction, which in turn can compete with metabolic vasodilator influences, and thus modulate alterations in coronary vascular resistance (Mohrman and Feigl, 1978).Although the existence of sympathetic coronary vasoconstrictor activity appears to be well documented, the physiological importance of such a mechanism remains unresolved.