Renal hemodynamic effects of captopril in anesthetized sodium-restricted dogs. Relative contributions of prostaglandin stimulation and suppressed angiotensin activity.

The mechanism of captopril-induced alterations in arterial pressure (AP), glomerular filtration rate (GFR), renal blood flow (RBF), and renal vascular resistance (RVR) was studied in pentobarbital anesthetized sodium-restricted dogs. In 7 dogs, captopril caused decreases in AP (16 +/- 3%) and RVR (46 +/- 5%), as well as increases in RBF (62 +/- 12%) and sodium excretion (399 +/- 73%). These responses were reversed by angiotensin II infusion at a rate sufficient to restore RBF to control levels. The captopril-induced increase in GFR (29 +/- 8%) was partially reversed by the intravenous angiotensin II infusion to a level not significantly different from control. In 5 dogs, indomethacin increased AP (10 +/- 2%) and RVR (38 +/- 8%); the slight decreases in RBF and GFR were not statistically significant. Subsequent captopril treatment decreased AP (20 +/- 3%) and RVR (42 +/- 4%), while RBF and GFR increased by 45 +/- 8% and 32 +/- 10%, respectively. These observations suggest that the renal response to captopril in sodium-restricted dogs is not dependent upon alterations in prostaglandin synthesis but, instead, is primarily due to diminished angiotensin II activity.