787-6 Hypotension Induced by Captopril in Patients with Primary Autonomic Failure Occurs Independently of Plasma Renin Levels and Sympathetic Nervous Activity

We have investigated the haemodynamic and hormonal responses to angiotensin converting enzyme inhibition in 12 patients with primary autonomic failure (AF, 5 pure autonomic failure, 7 multiple system atrophy) and 7 normal subjects. Measurements of blood pressure (BP), heart rate (HR), stroke distance (SO) and cardiac index (CI, continuous wave Doppler, forearm blood flow (FBF, strain gauge plethysmography) and digital skin blood flow (DSBF, laser Doppler flowmetry) were made non-invasively. Plasma renin activity (PRA) and noradrenaline (NGRAD) were measured before and at 30 min intervals after captopril (50 mg, oral). Basal supine BP was higher in AF compared to normals (p l 0.05). After captopril, mean BP fell in AF (117 ± 6 to 103 ± 5 mmHg, p l 0.05). but not in normals (99 ± 4 to 97 ± 5 mmHg, ns). HR was unchanged after captopril in both groups. The depressor response in AF was accompanied by a fall in SD (9.6 ± 1.2 to 7.6 ± 0.7 cm, p l 0.05) and in CI (676 ± 79 to 536 ± 65 cm/min, p l 0.05). SD and CI were unchanged after captopril in normals (SD, 7.7 ± 1.3 to 7.4 ± 0.6 cm; CI. 579 ± 117 to 571 ± 69 cm/min, both ns). There was no reduction in forearm or digital skin vascular resistance after captopril in either group. Basal PRA in AF was similar to normals, but did not rise after captopril (691 ± 217 to 681 ± 221 pg/ml/hr, ns), unlike normals (813 ± 103 to 1360 ± 290 pg/ml/hr, p l 0.05). NORAO was unchanged after captopril in both groups. We conclude that. captopril lowers blood pressure in AF, unlike normals. The depressor response in AF occurs independently of plasma renin levels and sympathetic nervous activity, suggesting that alternative mechanisms, including accumulation of bradykinin and prostaglandins, may be responsible.