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Angiotensin converting enzyme inhibition lowers blood pressure in patients with primary autonomic failure independently of plasma renin levels and sympathetic nervous activity.

The haemodynamic and neurohormonal responses to the angiotensin converting enzyme (ACE) inhibitor captopril were studied in 12 patients with primary autonomic failure; seven had multiple system atrophy and five had pure autonomic failure. Basal supine mean arterial blood pressure was higher in the patients with multiple system atrophy than in those with pure autonomic failure and the normal subjects. Basal plasma noradrenaline levels were normal in the patients with multiple system atrophy, but lower in those with pure autonomic failure. Captopril lowered the mean arterial pressure in the patients with multiple system atrophy and pure autonomic failure but not in the normal subjects. In the patients with multiple system atrophy and pure autonomic failure, captopril lowered the cardiac output and the stroke volume. Forearm vascular resistance was unchanged. No significant changes occurred in the normal subjects. Plasma renin activity was unchanged after captopril in the patients with autonomic failure, but rose in the normal subjects. Plasma noradrenaline was unchanged in all groups after the administration of captopril. We conclude that captopril lowers the mean arterial pressure in patients with multiple system atrophy and pure autonomic failure. After the administration of captopril there is a reduction in cardiac output, secondary to a fall in stroke volume. The vasodepressor response to captopril in patients with autonomic failure is not related to the basal level of plasma renin activity or sympathetic nervous activity, indicating that the hypotensive effects of bradykinin or prostaglandins, or both, may contribute.