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

Pamela K. Carmines, László Rosivall, Margaret F. Till, L. Gabriel Navar

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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.

Original languageEnglish
Pages (from-to)281-287
Number of pages7
JournalKidney and Blood Pressure Research
Issue number6
Publication statusPublished - Jan 1 1983



  • Angiotensin
  • Captopril
  • Glomerular filtration rate
  • Prostaglandin
  • Renal vascular resistance

ASJC Scopus subject areas

  • Nephrology
  • Cardiology and Cardiovascular Medicine

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