Abstract
Angiotensin II was blocked by its inhibitor Sarl-Ala8- Angiotensin II /Eaton Lab. Horwick NY/ in 2 Bratter's syndromes: case I without and case II with the salt loosing form. Infusion of the inhibitor was performed during 6h at progressive rate /l to looug/kg/mn/ in case I and during 4h at constant rate /loo/ug/kg/ran/ in case II. Blood pressure /BP/, plasma renin activity /PRA/, Aldosterone /A/, ACTH, Cortisol /F/, Na and K levels, urinary Na and K excretion /as related to creatinine clearence /were studied hourly. In both cases PRA increased sharply but changes were different for the other parameters. In case I, BP, ACTH and F remained stable; A decreased; in urine Na increased while K decreased with opposite changes in plasma. In case II there was a transient decrease in BP; ACTH, F and A raised sharply during the 1rst h followed by a progressive decrease; no change occured in Na and K excretion; plasma Na and K showed a small decrease. Conclusion: In case I blockade of Angiotensin induced a basal hyperreninemia and hyperaldosteronemia was an efficient compensatory mechanism for a primary urinary Na leakage. In case II this compensatory mechanism was inefficient.
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David, L., Sann, L., Sassard, J. et al. EFFECT OF BLOCKADE OF ANGIOTENSIN II BY SAR 1-ALA 8- ANGIOTENSIN II IN BARTTER'S SYNDROME. Pediatr Res 9, 865 (1975). https://doi.org/10.1203/00006450-197511000-00080
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DOI: https://doi.org/10.1203/00006450-197511000-00080