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Coronary vascular responses to stimulation of chemoreceptors were studied in anesthetized, artificially ventilated dogs. The circumflex coronary artery was perfused at constant flow so that changes in perfusion pressure reflected changes in coronary resistance. Practolol, a myocardioselective beta-receptor antagonist, and pacing were used to minimize indirect effects of myocardial responses on coronary resistance. Carotid and aortic injections of nicotine produced decreases in coronary perfusion pressure averaging −21 mm Hg and −22 mm Hg, respectively. Decreases with carotid and aortic injections of cyanide averaged −8 mm Hg and −17 mm Hg, respectively. These coronary dilator responses were abolished by bilateral vagotomy or atropine. Changes in perfusion pressure with carotid injections of nicotine averaged +3 mm Hg after vagotomy and +2 mm Hg after administration of atropine. The coronary dilator responses to carotid chemoreceptor stimulation were accompanied by increases in coronary sinus Po2 in five studies and no change in two studies. Carotid sinus nerve stimulation caused abrupt and sustained coronary vasodilatation. After vagotomy or administration of atropine, the response to carotid sinus nerve stimulation was no longer abrupt but occurred gradually, suggesting that a component of the reflex response was blocked. These studies indicate that stimulation of chemoreceptors activates a vagal cholinergic vasodilator pathway to coronary vessels in the dog. Activation of this pathway appears also to contribute to reflex coronary responses to stimulation of baroreceptors.

Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION