Carotid chemoreceptor reflex activation (CCRA) has been previously shown to result in intense α-adrenergic peripheral vasoconstriction, a biphasic coronary vascular response characterized by an early vasodilation and a late α-adrenergic vasoconstriction, and a cholinergic increase in cardiac cycle length in normal conscious dogs. In the present study, we investigated the extent to which these reflex cardiovascular responses to CCRA are modified after the development of pressure-overload right ventricular (RV) hypertrophy induced by chronic (9-12 mo) pulmonary arterial stenosis. With heart rate constant and respiration allowed to vary spontaneously, the magnitude of the late CCRA-induced (intracarotid nicotine) increase (P < 0.01) in right coronary resistance was markedly attenuated (P < 0.01) in conscious dogs with RV hypertrophy [0.29 ± 0.07 (SE) mmHg.ml-1.min] compared with normal dogs (1.87 ± 0.36). When respiration was controlled to eliminate pulmonary inflation reflex activation, the late CCRA-induced increase (P < 0.01) in right coronary resistance was still found to be depressed (P < 0.01) in the RV hypertrophy group (1.11 ± 0.20 mmHg.ml-1.min) compared with normal dogs (3.65 ± 0.75). This late CCRA-induced right coronary vasoconstriction was not potentiated by β-adrenergic receptor blockade but was abolished (P < 0.01) by α-adrenergic receptor blockade. In contrast to the depressed right coronary vasoconstriction, the CCRA-induced α-adrenergic constriction (P < 0.01) of the iliac arterial vascular bed was similar in both groups, and the cholinergic increase (P < 0.01) in cardiac cycle length was enhanced (P < 0.01) in the RV hypertrophy group compared with normal dogs. These results indicate that the development of RV hypertrophy is not characterized by a generalized depression in reflex cardiovascular control. Moreover, the attenuated CCRA-induced right coronary vasoconstriction appears to be the result of a selective depression in α-adrenergic vasoconstrictor capacity of the coronary vasculature supplying the hypertrophied right ventricle, whereas reflex α-adrenergic constrictor capacity of the line artery is preserved.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1983|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)