Cholinergic baroreflex vasodilatation: defect in heart transplant recipients due to denervation of the ventricular baroreceptor.

Afferent denervation of the ventricular baroreceptor may impair reflex vasodilatation after heart transplantation. This may alter the regulation of blood pressure and contribute to arterial hypertension. A baroreceptor-loading procedure was performed in 23 heart transplant recipients with cyclosporine A immunosuppression and 11 control subjects using a continuous infusion of increasing doses of angiotensin II (15 and 30 ng/kg.min). After m-cholinoceptor blockade the procedure was repeated in order to study the contribution of cholinergic effects on vasodilatation in humans. Instantaneous vascular resistance was calculated as the ratio of mean blood pressure to stroke volume as evaluated by echocardiography. When heart transplant recipients were compared with control subjects, infusion of 30 ng/kg.min of angiotensin II resulted in an increase in mean blood pressure of 43 +/- 20 vs 31 +/- 13 mm Hg (p less than 0.05) and an increase in instantaneous resistance of 1.21 +/- 0.61 vs 0.65 +/- 0.38 mm Hg/ml (p less than 0.01), respectively. M-cholinoceptor blockade with atropine (0.015 mg/kg) did not produce any change in blood pressure or resistance response to angiotensin II in heart transplant recipients. However, m-cholinoceptor blockade resulted in a significantly increased blood pressure and resistance response to angiotensin II in control subjects, which was similar to the response in heart transplant recipients to angiotensin II alone: The increase in mean blood pressure during administration of 30 ng/kg.min angiotensin II amounted to 47 +/- 11 mm Hg, and the increase in instantaneous resistance to 1.13 +/- 0.48 mm Hg/ml (for both, p less than 0.001 vs control subjects without atropine; p = not significant vs heart transplant recipients).(ABSTRACT TRUNCATED AT 250 WORDS)