Carotid sinus baroreceptor control of right coronary circulation in normal, hypertrophied, and failing right ventricles of conscious dogs.

Tlie right coronary vascular response to bilateral carotid occlusion (BCO) was assessed in normal, conscious dogs and also in dogs with right ventricular (RV) hypertrophy alone or in combination with right heart failure, induced by chronic (5-7 months) pulmonary artery stenosis.In normal, conscious dogs with intact adrenergic neural activity and with heart rate held constant by electrical pacing, BCO increased (P < 0.01) mean aortic pressure (33 ± 4%) and induced only minor changes in RV hemodynamics, but no change in right coronary blood flow (4 ± 3%), and a significant increase (P < 0.01) in right coronary resistance (32 ± 5%)./J-Adrenergic receptor blockade did not unmask a further right coronary constrictor response to BCO.However, combined a-and /3-adrenergic receptor blockades significantly reduced (P < 0.02) the BCO-lnduced Increase in right coronary resistance.When we raised m m i aortic pressure by an amount similar (34 ± 8%) to that which occurred with BCO, but in this case by hydraulically constricting the ascending thoracic aorta in conscious dogs pretreated with a ganglionlc blocker, right coronary blood flow rose (P < 0.01) 55 ± 8%.The BCOinduced increase in right coronary resistance was greatly attenuated (P < 0.O1) in dogs with RV hypertrophy alone, and further depressed (P < 0.01) in dogs with RV failure.Thus, in the normal, conscious dog with intact adrenergic neural activity, BCO elicits an increase hi right coronary resistance which is: (1) not the result of right coronary autoregulation, (2) not enhanced by /3-adrenergic receptor blockade, and (3) largely due to a-adrenergic vasoconstriction.Furthermore, the BCO-induced right coronary constriction is diminished in dogs with RV hypertrophy alone, and further depressed in dogs with RV hypertrophy and failure.Ore Res 49:1339-1349, 19S1CAROTID sinus hypotension initiates a complex sequence of events which can exert multiple and counteracting effects on coronary vascular dynamics.For example, carotid sinus hypotension has been shown previously to elicit net increases in left coronary blood flow in anesthetized preparations with adrenergic neural activity intact (Feigl, 1968;Bond and Green, 1969; DiSalvo et al., 1971;Mohrman and Feigl, 1978).However, when both changes in myocardial metabolic demand initiated by the hemodynamic response to carotid sinus hypotension and also any direct /8-adrenergically mediated vasodilation were limited by administering a ^-adrenergic antagonist, bilateral carotid occlusion (BCO) elicited an increase in calculated left coronary vascular resistance (Feigl, 1968; DiSalvo et aL, 1971;Powell and Feigl, 1979).This increase in left coronary resistance has been attributed to reflex