Hypertension, Vol 13, 749-753, Copyright © 1989 by American Heart Association
H Saito, M Nakamaru, T Ogihara, H Rakugi, Y Kumahara, K Shimamoto, M Miyazaki and T Inagami
The direct effects of a renin inhibitor, N-acetyl-pepstatin and five
angiotensin converting enzyme inhibitors, captopril and the active diacid
forms of enalapril, ramipril, cilazapril, and CS-622, on the vascular
renin-angiotensin system were examined in isolated perfused rat mesenteric
arteries. Vascular renin activity and angiotensin II (Ang II) released into
the perfusate were determined. Infusion of N- acetyl-pepstatin (5 X
10(-8)-5 X 10(-6) M) suppressed vascular renin activity and Ang II release
dose dependently. Isoproterenol (10(-6) M) induced a 135 +/- 30% increase
in Ang II release from the basal value. N-Acetyl-pepstatin (5 X 10(-6) M)
suppressed isoproterenol-induced Ang II release. Infusions of 5 X 10(-6) M
captopril and the diacid forms of enalapril, ramipril, cilazapril, and
CS-622 by themselves had little effect on Ang II release, but concomitant
infusion of isoproterenol with these angiotensin converting enzyme
inhibitors significantly decreased Ang II release (71 +/- 21%, 51 +/- 40%,
8 +/- 21%, 69 +/- 24%, and 44 +/- 29% increase, respectively, from the
basal values). These results indicate that N-acetyl-pepstatin suppresses
the vascular renin-angiotensin system. This effect may in part contribute
to the hypotensive actions of renin inhibitors. Although angiotensin
converting enzyme inhibitors also suppress locally generated Ang II, the
mechanism and physiological significance still remain to be clarified.
ARTICLES
Renin inhibitor and converting enzyme inhibitors suppress vascular angiotensin II
Department of Geriatric Medicine, Osaka University Medical School, Japan.
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1989 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |