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ROLE OF THE KALLIKREIN‐KININ SYSTEM IN THE RENAL EFFECTS OF ANGIOTENSIN‐CONVERTING ENZYME INHIBITION IN ANAESTHETIZED DOGS
Author(s) -
Clappison B. H.,
Anderson W. P.,
Johnston C. I.
Publication year - 1981
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1981.tb00758.x
Subject(s) - captopril , kinin , endocrinology , medicine , vasodilation , renin–angiotensin system , kallikrein , bradykinin , renal blood flow , renal circulation , angiotensin ii , angiotensin converting enzyme , blood pressure , chemistry , kidney , antagonist , receptor , enzyme , biochemistry
SUMMARY 1. Administration of captopril (1.5mg/kg i.v.) to anaesthetized dogs was associated with an increase in renal blood flow of 56 ml min ‐1 (s.e.m. = 13, n = 9) despite a significant fall of 17 mmHg (s.e.m. = 5, n = 9) in mean arterial pressure. 2. Treatment of dogs with the angiotensin receptor antagonist, Sar'lle 8 ‐angiotensin II (2.5 fxgjkg per min i.v.), or the cyclo‐oxygenase inhibitor indo‐methacin (10 mg/kg i.v.) did not prevent the renal vasodilation and hypotension following angiotensin‐converting enzyme inhibition. This suggests that these effects are neither solely due to inhibition of the renin‐angiotensin system nor mediated by prostaglandins. 3. Increased urinary kinin excretion, possibly reflecting increased renal concentrations of kinins, accompanied the renal vasodilation after both captopril and renal artery occlusion. 4. The kallikrein‐kinin system may play a role in the regulation of the renal vasculature in anaesthetized dogs.