Carotid baroreceptor reflex coronary vasodilation in the dog.

Abstract

SUMMARY. The hypothesis that neurally mediated coronary vasodilation occurs as part of the carotid baroreceptor reflex was investigated. The left main coronary artery was cannulated and perfused at constant pressure (100 mm Hg) in closed-chest, chloralose-anesthetized dogs. The heart was paced at a constant rate between 60 and 70 beats/min after atrioventricular heart block. Propranolol (1 mg/kg) was given to prevent j3-receptor-mediated alterations in contractility. Aortic blood pressure was stabilized with a blood reservoir. The aortic depressor nerves were cut bilaterally to prevent the buffering influence of aortic arch baroreceptors on the carotid baroreceptor reflex. The carotid sinuses were vascularly isolated and perfused with arterial blood at controlled pressures. Under these conditions, a step change in carotid sinus pressure from 70 to 210 mm Hg produced a 0.29 ml/min per g increase in coronary flow above control and a 10 mm Hg increase in coronary sinus blood oxygen tension. A step in carotid sinus pressure from 70 to 150 mm Hg resulted in a flow increase of 0.13 ml/min per g and a coronary sinus oxygen tension increase of 5.3 mm Hg relative to prestimulation values. Atropine (0.5 mg/kg, iv) blocked most of the reflex coronary vasodilation, indicating a parasympathetic component, and the addition of adrenergic a-receptor blockade with phenoxybenzamine (0.25 mg/kg, ic) abolished the remaining response, demonstrating sympathetic participation. The reflex nature of the coronary response was confirmed with carotid sinus denervation and vagotomy. It is concluded that carotid sinus hypertension results in a graded reflex neural coronary vasodilation independent of myocardial metabolic factors. The major component is due to activation of parasympathetic coronary vasodilator fibers, but there is also inhibition of sympathetic vasoconstrictor fibers. (Circ Res 56: 486-495, 1985) PREVIOUS studies have demonstrated that adrenergic a-receptor coronary vasoconstriction can be reflexly elicited by carotid sinus hypotension (Feigl, 1968(Feigl, , 1983DiSalvo et al., 1971;Limet et al., 1975;Powell and Feigl, 1979;Ely et al., 1981). However, the reflex response to carotid sinus hypertension is less clear. Both coronary vasoconstriction (DiSalvo et al., 1971) and coronary vasodilation (Limet et al., 1975) have been observed during acute elevations in carotid sinus pressure. Coronary vasodilation during the elevation of aortic pressure has also been attributed to the carotid baroreflex (White et al., 1976). Electrical stimulation of the afferent carotid sinus nerve has been employed to mimic carotid sinus hypertension, and either coronary vasoconstriction (Falicov et al., 1970) or vasodilation (Vatner et al., 1970;Hackett et al., 1972;Religa et al., 1972;Solti et al., 1975) has been observed. However, it is difficult to equate a given nerve stimulation frequency with a carotid sinus pressure stimulus that physiologically activates baroreceptors. Furthermore, electrical stimulation of carotid sinus baroreceptor affe...

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

“…The coronary vasodilatation seen in the present study is similar to that which has PULMONARY CHEMOREFLEX AND CORONAR Y RESISTANCE 287 been observed previously during carotid sinus nerve stimulation (Hackett, Abboud, Mark, Schmid & Heistad, 1972), peripheral chemoreceptor stimulation (Hashimoto, Igarashi, Uei & Kumakura, 1964;Vatner & McRitchie, 1975;Vatner, 1983;Murray, Lavallee & Vatner, 1984), carotid sinus baroreceptor stimulation (Ito & Feigl, 1985), and the Bezold-Jarish reflex (Feigl, 1975). Further, the neurohumoral basis for the changes in coronary resistance evoked by capsaicin in the present study is comparable to that seen in previous studies.…”

The effect of distension of the urinary bladder on coronary blood flow in anesthetized dogs

“…The effect of atropine and bretylium tosylate or the effect of vagotomy and bretylium tosylate, suggest that the withdrawal of activity in efferent vagal pathways contributed less to the magnitude of the coronary vasoconstriction than the sympathetic pathways. Previous reports regarding the reflex effect on the coronary circulation to stimulation of carotid sinus baroreceptors have indicated a major contribution of vagal pathways (Ito & Feigl, 1985). These differences between the contribution of constituents of efferent pathways have occurred despite the sharing of the same groups of efferent sympathetic and vagal cardiac nerve fibres by the bladder distension reflex and carotid sinus baroreflex (Hassan et al 1987a, b).…”

“…Efferent cardiac nerves are believed to be involved in the reflex changes in coronary blood flow caused by stimulation of carotid sinus baroreceptors, atrial and ventricular receptors (e.g. Feigl, 1983;Ito & Feigl, 1985; Coleridge, Coleridge, Clozel, Hoffman, Roberts & Pisarri, 1987;Drinkhill, Kaye & Mary, 1989a).…”

Reflex coronary vasodilation evoked by chemical stimulation of cardiac afferent vagal C fibres in dogs.

“…It is unlikely, therefore, that ischaemic stimulation of arterial chemoreceptors was responsible for the coronary vasodilatation of the present experiments. Clearly, arterial baroreceptors were not responsible for the reflex increase in coronary blood flow because coronary vascular resistance varies inversely with carotid sinus pressure (Ito & Feigl, 1985b).…”