Effect of captopril on the systemic and renal responses to acute isotonic volume expansion in normal man.
Systemic, humoral and renal responses to isotonic volume expansion (VE, 1800ml in 3 hours) were assessed in normal subjects before and during captopril administration (CEI). Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP) unmasked the volume-dependence of MAP since during captopril administration MAP increased linearly during volume expansion (+18.7 +/- 3.8% at the end of VE). In addition, captopril prevented the fall in plasma aldosterone produced by VE but did not modify the natriuretic response to saline. These results demonstrate that circulating angiotensin II is not an important determinant of the natriuretic response to volume expansion in normal man. However, a role for intrarenal renin cannot be excluded.
D000328:Adult; D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects*; D001810:Blood Volume; D002216:Captopril / Q000494:pharmacology*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000652:urine; D011392:Proline / Q000031:analogs & derivatives*; D012964:Sodium / Q000652:urine; D012965:Sodium Chloride
D012965:Sodium Chloride; D000450:Aldosterone; D011392:Proline; D002216:Captopril; D012964:Sodium; D011188:Potassium