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 Po 2 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.

Experiments were done to characterize the vascular responses to stimulation of aortic and carotid chemoreceptors and to identify the efferent components of the sympathetic system which are activated in different vascular beds. The chemoreceptors were stimulated with nicotine and cyanide in anesthetized and artificially ventilated dogs. The gracilis muscle and hindpaw were isolated and perfused with blood at constant flow. Changes in perfusion pressure reflected changes in total vascular resistance, and changes in small vein pressure reflected changes in venous resistance. The results indicate that stimulation of carotid and aortic chemoreceptors activates selectively efferent adrenergic constrictor fibers supplying prevenous resistance vessels in the gracilis muscle and venous resistance vessels in the paw. In contrast, there was a dilatation of prevenous resistance vessels in the paw caused by activation of efferent sympathetic dilator fibers and not by withdrawal of sympathetic constrictor tone. The dilatation was not mediated through the release of acetylcholine, histamine, or bradykinin nor through beta receptors. Bilateral denervation of the carotid sinus and body and bilateral vagotomy abolished the reflex responses caused by injections of the chemicals. These responses were not the result of activation of baroreceptors since they were not reproduced during electrical stimulation of the carotid sinus nerve.