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1 Department of Pharmacognosy and Pharmacology, College of Pharmacy, University of Florida, Gainesville, Florida
The interaction of alpha and beta adrenergic receptors in the myocardium and the activity of quinidine were investigated employing a modified Anderson-Craver coronary perfusion apparatus with the rat heart and measuring the change in the effective refractory period (ERP) induced by the various drug treatments. The action of quinidine on the ERP was enhanced in the presence of alpha adrenergic blockade or stimulation and decreased in the presence of beta adrenergic blockade or stimulation. The effect of quinidine (4 mg/liter) on the ERP of the rat heart was potentiated in the presence of phenoxybenzamine (50 µg/liter) or phentolamine (100 µg/liter). The ERP was increased 165 and 195%, respectively, over that of the quinidine-treated control hearts (P < .01). In the presence of 250 µg/liter of norepinephrine, quinidine (8 mg/liter) increased the refractory period 69% over that of the controls (P < .01). When propranolol (50 µg/liter) was employed in the presence of 8 mg/liter of quinidine, the ERP was decreased 25% (P < .05) from the quinidine control hearts. In the presence of 25 µg/liter of isoproterenol, 8 mg/liter of quinidine decreased the ERP 27% from the controls (P < .05). The results of these experiments suggest that alpha adrenergic receptors, as well as beta adrenergic receptors, are present in the rat myocardium and that these receptors can modify the activity of quinidine on the ERP of the rat heart.
Submitted on October 31, 1967