Local regulation of vascular tone by bradykinin and angiotensin converting enzyme inhibitors

Part of the vasodilator response to angiotensin converting enzyme (ACE) inhibitors depends on stimulation of bradykinin receptors, but in most studies the anticipated increase in plasma kinin concentration during ACE inhibition was not detected. We investigated the role of local ACE inhibition on en...

Full description

Saved in:
Bibliographic Details
Published inEuropean heart journal Vol. 14 Suppl I; p. 154
Main Authors Auch-Schwelk, W, Kuchenbuch, C, Claus, M, Walther, B, Bossaller, C, Friedel, N, Graf, K, Gräfe, M, Fleck, E
Format Journal Article
LanguageEnglish
Published England 01.11.1993
Subjects
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals
Bradykinin - physiology
Cattle
Coronary Vessels - drug effects
Dose-Response Relationship, Drug
Drug Synergism
Endothelium, Vascular - drug effects
Endothelium, Vascular - secretion
Humans
In Vitro Techniques
Nitric Oxide - secretion
Renal Artery - drug effects
Tail - blood supply
Vasodilation - drug effects
Vasodilation - physiology
Online AccessGet more information

Cover

More Information
Summary:Part of the vasodilator response to angiotensin converting enzyme (ACE) inhibitors depends on stimulation of bradykinin receptors, but in most studies the anticipated increase in plasma kinin concentration during ACE inhibition was not detected. We investigated the role of local ACE inhibition on endothelial control of vascular tone. Rings of bovine coronary, renal and tail arteries, as well as human coronary arteries, were mounted in organ chambers so that the isometric force could be recorded. The ACE inhibitors, captopril, fosinoprilat, enalaprilat, lisinopril, and ramiprilat alone had no affect on the vascular tone of bovine coronary arteries with endothelium. However, these ACE inhibitors did potentiate relaxations to bradykinin and the slowly degradable bradykinin derivative [Hyp3-Tyr(Me)8]-bradykinin (3 x 10(-11) M). A similar response was observed in human coronary arteries. The response was not observed in rings of any vessel without endothelium, or after incubation with nitro-L-arginine (10(-4) M), or the bradykinin2-receptor antagonists Hoe 140 (10(-8) M). The sensitivity to bradykinin was higher and the potentiating effect of ACE inhibition larger in the bovine coronary artery than in the renal and tail artery. Thus, ACE inhibition causes selective coronary vasodilation by potentiating the bradykinin-induced release of nitric oxide from the endothelium. The related mechanism underlying these effects must occur at the surface or within the arterial wall and seems to be independent of the degradation of the kinins.
ISSN:0195-668X