Bradykinin-Induced Vasodilation Is Impaired at the Atherosclerotic Site but Is Preserved at the Spastic Site of Human Coronary Arteries In Vivo

作者：Takeshi Kuga, Kensuke Egashira, Masahiro Mohri, Hiroyuki Tsutsui, Yasuhiko Harasawa, Yoshitoshi Urabe, Shin‐ichi Ando, Hiroaki Shimokawa, Akira Takeshita · 发表于：Circulation · 年份：1995 · DOI：10.1161/01.cir.92.2.183 · 被引用次数：79 · 研究领域：Coagulation, Bradykinin, Polyphosphates, and Angioedema、Coronary Interventions and Diagnostics、Cerebrovascular and Carotid Artery Diseases

BACKGROUND: Bradykinin causes endothelium-dependent vasodilation of isolated human coronary arteries in vitro. However, the effect of bradykinin on vasomotion of human coronary arteries in vivo has not been studied. The aim of this study was to examine whether bradykinin-induced vasodilation is altered at the atherosclerotic or spastic site of human coronary arteries in vivo. METHODS AND RESULTS: The effect of bradykinin on vasomotion of epicardial coronary arteries was evaluated in 8 patients with normal coronary arteries (control group), 14 patients with organic coronary stenosis (coronary artery disease [CAD] group), and 8 patients with vasospastic angina (VSA group). Changes in the diameter of epicardial coronary artery were assessed by quantitative coronary arteriography. Intracoronary administration of bradykinin at graded doses (60, 200, and 600 ng) dilated epicardial coronary arteries without altering arterial pressure or heart rate in all patients of either group. In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction. The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean +/- SD: 6 +/- 6%, 11 +/- 9%, and 15 +/- 9%) were comparable to that (3 +/- 6%, 8 +/- 8%, and 13 +/- 9%) at the site with acetylcholine-induced constriction. In the CAD group, vasomotor responses of the stenotic site (% diameter stenosis...