TY - JOUR
T1 - Bradykinin-induced vasodilation of human coronary arteries in vivo
T2 - Role of nitric oxide and angiotensin-converting enzyme
AU - Kuga, Takeshi
AU - Mohri, Masahiro
AU - Egashira, Kensuke
AU - Hirakawa, Yoji
AU - Tagawa, Tatsuya
AU - Shimokawa, Hiroaki
AU - Takeshita, Akira
N1 - Funding Information:
This study was supported in part by a Grant-in Aid for Scientific Research from the Japanese Ministry of Education, Science and Culture, Tokyo, Japan, and by a research grant from the Kanae Foundation of Research for New Medicine, Tokyo, Japan.
PY - 1997/7
Y1 - 1997/7
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.
AB - 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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U2 - 10.1016/S0735-1097(97)00112-5
DO - 10.1016/S0735-1097(97)00112-5
M3 - Article
C2 - 9207629
AN - SCOPUS:0030740673
SN - 0735-1097
VL - 30
SP - 108
EP - 112
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 1
ER -