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Carotid Sinus Baroreceptor Control of Right Coronary Circulation in Normal, Hypertrophied, and Failing Right Ventricles of Conscious Dogs

The 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%). β-Adrenergic receptor blockade did not unmask a further right coronary constrictor response to BCO. However, combined α- and β-adrenergic receptor blockades significantly reduced (P < 0.02) the BCO-lnduced Increase in right coronary resistance. When we raised mm 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 BCO- induced 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 β-adrenergic receptor blockade, and (3) largely due to α-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.