alpha-Adrenoceptor attenuation of the coronary vascular response to severe exercise in the conscious dog.
Author(s) -
Paul A. Murray,
Stephen F. Vatner
Publication year - 1979
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/01.res.45.5.654
Subject(s) - alpha (finance) , cardiology , medicine , adrenergic receptor , alpha 2 adrenergic receptor , endocrinology , receptor , surgery , patient satisfaction , construct validity
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 β-receptor blockade (propranolol, 1 mg/kg), α-receptor blockade (phentolamine, 1-2 mg/kg), or combined β and α-receptor blockades. Heart rate was held constant by electrical stimulation throughout the exercise period. After α-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 β-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 α and β 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 α-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 α 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, 1979
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