AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 3 481-R489, Copyright © 1995 by American Physiological Society

ARTICLES

ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure

W. Boemke, E. Seeliger, L. Rothermund, M. Corea, R. Pettker, G. Mollenhauer and H. W. Reinhardt
Arbeitsgruppe Experimentelle Anasthesie, Universitatsklinikum Rudolf Virchow--Charlottenburg, Freie Universitat Berlin, Germany.

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.

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