Acute and chronic converting enzyme inhibition reduces the vasomotor response to reflex sympathetic activation in man.

Several lines of evidence indicate that angiotensin II (ANG II) may potentiate the vascular response to sympathetic stimulation. However, there are no clear signs that this action of ANG II is physiologically relevant in man. To investigate this problem, we used the lower body negative pressure technique (LBNP, -15 mmHg) to deactivate cardiopulmonary receptors and reflexly stimulate the sympathetic nervous system. The haemodynamic (changes in blood pressure, heart rate, central venous pressure, forearm blood flow) and humoral effects [changes in plasma noradrenaline (PNA) and plasma renin activity (PRA)] of this manoeuvre were examined before and after blockade of angiotensin formation achieved by the administration of the converting enzyme inhibitor, captopril. Studies were performed in patients with essential hypertension in control conditions and after acute and chronic captopril treatment. We found that the reduction in forearm blood flow induced by LBNP was significantly diminished after acute and chronic captopril in spite of the fact that the fall in central venous pressure and the increases in PNA were similar to those observed in control conditions. In contrast, the response of renin to LBNP was enhanced, at least after acute captopril administration. These findings suggest that efficiency of the reflexes originating from the cardiopulmonary receptors is impaired after captopril. Angiotensin II contributes to the vasoconstrictive ability of the sympathetic nervous system, either through a direct vascular action or by enhancing the vascular responsiveness to noradrenaline stimulation. However, this sympathetic facilitatory action of ANG II does not appear to be extended on the adrenergic mechanisms which regulate renin release.