Possible mechanisms involved in the coronary vasodilatory response to dopamine.
Dopamine increased coronary blood flow in the dog heart pretreated with alpha-adrenoceptor blocking agents. The coronary vasodilator response was completely inhibited by indomethacin when pretreated with propranolol in addition to alpha blockade. The coronary vasodilation exerted by sodium nitrite was potentiated by indomethacin and adrenergic blockade. In coronary arterial strips, dopamine produced a contraction which was abolished by phenoxybenzamine. Dopamine elicited a dose-dependent relaxation in coronary arterial strips contracted previously by KC1 after pretreatment with phenoxybenzamine. The relaxation was potentiated by indomethacin; this effect was completely blocked by propranolol. Prostaglandin (PG)E1 produced a relaxing response but reduced the dopamine-induced relaxation. From the results it is suggested that beta-adrenoceptor stimulation and release of PG were involved in the coronary vasodilator response to dopamine. PG released by dopamine may increase coronary blood flow on the one hand and reduce beta-adrenoceptor stimulation by inhibiting adenyl cyclase on the other.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects*; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology*; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D011458:Prostaglandins E; D011433:Propranolol; D011188:Potassium; D004298:Dopamine; D007213:Indomethacin