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Abstract

Comparative effects of alpha-1 and alpha-2 adrenoceptors in modulation of coronary flow during exercise.

J R Strader, P A Gwirtz and C E Jones
Journal of Pharmacology and Experimental Therapeutics August 1988, 246 (2) 772-778;
J R Strader
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P A Gwirtz
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C E Jones
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Abstract

During submaximal exercise, an alpha adrenergic vasoconstriction that opposes metabolic dilation exists in the coronary circulation. Fifteen dogs were given i.c. injections of prazosin (0.5 mg) or yohimbine (0.7 mg) to determine the participation of alpha 1 and alpha 2 adrenoceptors in the vasoconstriction during exercise. All dogs were chronically instrumented to measure left circumflex blood flow, heart rate, regional left ventricular function and global left ventricular function. The experimental protocol consisted of a graded exercise regimen during which, at the highest level of exercise an alpha antagonist was given i.c. Exercise significantly increased heart rate, left ventricular pressure, dP/dt, systolic shortening and rate of shortening, and coronary blood flow. After the prazosin injection there was an increase in circumflex blood flow (25 +/- 3%) as well as regional (38 +/- 6%) and global (20 +/- 3%) contractile function. However, there was no change in circumflex blood flow or myocardial function after yohimbine. These data indicate that during exercise the sympathetic constrictor tone in the coronary circulation is mediated primarily by alpha 1 adrenoceptors, with little or no involvement from alpha 2 adrenoceptors.

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Journal of Pharmacology and Experimental Therapeutics
Vol. 246, Issue 2
1 Aug 1988
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Abstract

Comparative effects of alpha-1 and alpha-2 adrenoceptors in modulation of coronary flow during exercise.

J R Strader, P A Gwirtz and C E Jones
Journal of Pharmacology and Experimental Therapeutics August 1, 1988, 246 (2) 772-778;

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Abstract

Comparative effects of alpha-1 and alpha-2 adrenoceptors in modulation of coronary flow during exercise.

J R Strader, P A Gwirtz and C E Jones
Journal of Pharmacology and Experimental Therapeutics August 1, 1988, 246 (2) 772-778;
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