Ace inhibition prevents sodium and water retention and mabp
increase during servo-controlled reduction of renal perfusion
pressure.
Boemke, Willehad, Erdmann Seeliger, Lars Rothermund, Marcel Corea,
Reinhard Pettker, G[diaeresis]otz Mollenhauer, and H. Wolfgang Reinhardt.
Arbeitsgruppe Experimentelle An[umlaut]asthesie, Universit[umlaut]atsklinikum
Rudolf Virchow - Charlottenburg, Freie Universit[umlaut]at Berlin; D-14050
Berlin; Germany
APStracts 2:0046R, 1995.
Two groups of 6 dogs were studied during 4 control days or 4 days of
reduced renal perfusion pressure (rRPP), servo-controlled at a level
20 % below the individual dog_s 24-h MABP during control days, i.e.,
below the threshold for renin release. During rRPP days endogenous
activation of plasma aldosterone (PAC) and angiotensin II (ANG II)
was inhibited by the angiotensin converting enzyme inhibitor
captopril (rRPP+Capto). The dogs were kept on a high sodium and high
water intake. Unlike studies during rRPP alone, there was no Na and
water retention during rRPP+Capto. GFR dropped by about 9 %, MABP
remained in the range of control days. Plasma renin activity rose to
values 14times above controls, while PAC decreased by about 60 %.
Atrial natriuretic peptide remained in the range of controls. In
conclusion, ACE 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 ANG II and PAC levels.
Received 8 September 1993; accepted in final form 9 February
1995.
APS Manuscript Number R507-3.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.