1. Systemic, humoral and renal responses to isotonic volume expansion (1800 ml in 3 h) were assessed in normal subjects before and during captopril administration.
2. Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP), unmasked the volume-dependence of MAP, which increased linearly during volume expansion (+ 18.7 ± 3.8% at the end of volume expansion).
3. Captopril prevented the fall in plasma aldosterone produced by volume expansion but did not modify the natriuretic response to saline.
4. These results suggest that intrarenal rather than circulating angiotensin II may be one of the determinants of the natriuretic response to volume expansion in normal man.