Bradykinin-induced vasodilation of human coronary arteries in vivo: Role of nitric oxide and angiotensin-converting enzyme

Takeshi Kuga, Masahiro Mohri, Kensuke Egashira, Yoji Hirakawa, Tatsuya Tagawa, Hiroaki Shimokawa, Akira Takeshita

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Abstract

Objectives. The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)- induced dilation of human coronary arteries in vivo. Background. BK, produced by way of the kinin-kallikrein system, causes endothelium-dependent vasodilation. However, little is known about the mechanism of BK-induced dilation of coronary arteries in humans in vivo. Methods. The effects of an inhibitor of NO synthesis and of an ACE inhibitor on BK-induced coronary vasodilation were examined in 20 patients who had no significant atherosclerotic stenosis in the artery under study. Lumen diameters of the large epicardial coronary arteries and coronary blood flow (CBF) were measured by quantitative coronary arteriography and intracoronary Doppler technique. Results. Intracoronary infusion of BK (0.6 and 2.0 μg/min) increased coronary artery diameter and CBF with no change in arterial pressure or heart rate. The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p < 0.01) after pretreatment with N(G)- monomethyl-L-arginine (200 μmol) and were significantly increased (p < 0.01) after pretreatment with enalaprilat (50 μg). Conclusions. BK-induced dilation of human large epicardial and resistance coronary arteries is mediated by NO and increased by prior ACE inhibition.

Original languageEnglish
Pages (from-to)108-112
Number of pages5
JournalJournal of the American College of Cardiology
Volume30
Issue number1
DOIs
Publication statusPublished - Jul 1 1997

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Bradykinin
Peptidyl-Dipeptidase A
Vasodilation
Coronary Vessels
Nitric Oxide
Dilatation
Enalaprilat
Kallikrein-Kinin System
Angiotensin-Converting Enzyme Inhibitors
Endothelium
Arginine
Angiography
Arterial Pressure
Pathologic Constriction
Arteries
Heart Rate

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

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Bradykinin-induced vasodilation of human coronary arteries in vivo : Role of nitric oxide and angiotensin-converting enzyme. / Kuga, Takeshi; Mohri, Masahiro; Egashira, Kensuke; Hirakawa, Yoji; Tagawa, Tatsuya; Shimokawa, Hiroaki; Takeshita, Akira.

In: Journal of the American College of Cardiology, Vol. 30, No. 1, 01.07.1997, p. 108-112.

Research output: Contribution to journalArticle

Kuga, Takeshi ; Mohri, Masahiro ; Egashira, Kensuke ; Hirakawa, Yoji ; Tagawa, Tatsuya ; Shimokawa, Hiroaki ; Takeshita, Akira. / Bradykinin-induced vasodilation of human coronary arteries in vivo : Role of nitric oxide and angiotensin-converting enzyme. In: Journal of the American College of Cardiology. 1997 ; Vol. 30, No. 1. pp. 108-112.
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N2 - Objectives. The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)- induced dilation of human coronary arteries in vivo. Background. BK, produced by way of the kinin-kallikrein system, causes endothelium-dependent vasodilation. However, little is known about the mechanism of BK-induced dilation of coronary arteries in humans in vivo. Methods. The effects of an inhibitor of NO synthesis and of an ACE inhibitor on BK-induced coronary vasodilation were examined in 20 patients who had no significant atherosclerotic stenosis in the artery under study. Lumen diameters of the large epicardial coronary arteries and coronary blood flow (CBF) were measured by quantitative coronary arteriography and intracoronary Doppler technique. Results. Intracoronary infusion of BK (0.6 and 2.0 μg/min) increased coronary artery diameter and CBF with no change in arterial pressure or heart rate. The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p < 0.01) after pretreatment with N(G)- monomethyl-L-arginine (200 μmol) and were significantly increased (p < 0.01) after pretreatment with enalaprilat (50 μg). Conclusions. BK-induced dilation of human large epicardial and resistance coronary arteries is mediated by NO and increased by prior ACE inhibition.

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