Role of kinin and renal angiotensin ii blockade in acute effects of
ace inhibitors in low renin hypertension.
Naitoh, Mareo, Hiromichi Suzuki, Kouki Arakawa, Akira Matsumoto,
Atsuhiro Ichihara, Hiroto Matsuda, Eiji Kubota, Marohito Murakami,
Hidetomo Nakamoto, and Takao Saruta.
Department of Internal Medicine, School of Medicine, Keio
University, Tokyo, Japan 160
APStracts 3:0378H, 1996.
In conscious deoxycorticosterone acetate (DOCA)-salt hypertensive
dogs, angiotensin converting enzyme (ACE) inhibitors, captopril and
imidaprilat, significantly decreased mean arterial pressure (MAP),
accompanied with significant increases in urine flow rate (UFR),
effective renal plasma flow (ERPF), glomerular filtration rate (GFR)
and urinary sodium excretion (UNaV). However, the angiotensin type 1
(AT1) receptor antagonist, losartan caused a significant increase
only in UNaV without significant changes in MAP, UFR, ERPF and GFR.
Simultaneous infusion of a bradykinin receptor antagonist inhibited
the ACE inhibitor-induced reduction in MAP and increase in ERPF.
DOCA-salt treatment markedly suppressed plasma angiotensin II
concentration (P<0.001), although it decreased renal angiotensin
II content only slightly (P<0.05). Comparison of the expression
of renal AT1 receptor mRNA between control kidneys and DOCA-salt
hypertensive kidneys revealed no significant change. These results
suggest that, in low renin hypertension, inhibition of the relatively
maintained angiotensin II production in the kidney participates in
the natriuretic action of ACE inhibitors. However, hypotensive and
other renal effects are mainly due to the action of bradykinin.
Received 27 February 1996; accepted in final form 21 August 1996.
APS Manuscript Number H193-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996