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脑钠肽的冠状动脉舒张作用:在冠状动脉传导动脉和阻力动脉中的作用机制

Coronary vasodilator effects of BNP: mechanisms of action in coronary conductance and resistance arteries.

作者信息

Zellner C, Protter A A, Ko E, Pothireddy M R, DeMarco T, Hutchison S J, Chou T M, Chatterjee K, Sudhir K

机构信息

The Vascular Research Laboratory, Division of Cardiology, University of California at San Francisco, San Francisco 94143-0124, California.

出版信息

Am J Physiol. 1999 Mar;276(3):H1049-57. doi: 10.1152/ajpheart.1999.276.3.H1049.

DOI:10.1152/ajpheart.1999.276.3.H1049
PMID:10070091
Abstract

Brain natriuretic peptide (BNP), a hormone secreted predominantly in ventricular myocytes, may influence coronary vascular tone. We studied the coronary vasodilatory response to BNP under physiological conditions and after preconstriction with endothelin-1 (ET-1) in anesthetized pigs. Average peak-flow velocity (APV) was measured using intracoronary Doppler, and cross-sectional area (CSA) was measured using intravascular ultrasound. Coronary blood flow (CBF) was calculated. Intracoronary BNP induced dose-dependent increases in CSA, APV, and CBF similar in magnitude to those induced by nitroglycerin (NTG). The magnitude of BNP-induced vasodilation was accentuated after preconstriction with ET-1. Pretreatment with either the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester or the cyclooxygenase inhibitor indomethacin attenuated the coronary vasodilator effect of BNP in resistance arteries without influencing epicardial vasodilation. Pretreatment with the ATP-sensitive potassium-channel blocker glibenclamide enhanced epicardial vasodilation in response to BNP. We conclude that BNP exerts coronary vasodilator effects, predominantly in epicardial conductance vessels. An accentuated vasodilatory response to BNP occurs in ET-1-preconstricted arteries. BNP-induced vasodilation in coronary resistance arteries may be partially mediated via nitric oxide and/or prostaglandin release.

摘要

脑钠肽(BNP)是一种主要由心室肌细胞分泌的激素,可能影响冠状动脉血管张力。我们在麻醉猪身上研究了生理条件下以及用内皮素-1(ET-1)预收缩后BNP对冠状动脉的舒张反应。使用冠状动脉内多普勒测量平均峰值流速(APV),并使用血管内超声测量横截面积(CSA)。计算冠状动脉血流量(CBF)。冠状动脉内注射BNP可引起CSA、APV和CBF呈剂量依赖性增加,其幅度与硝酸甘油(NTG)引起的相似。在用ET-1预收缩后,BNP诱导的血管舒张幅度增大。用一氧化氮合酶抑制剂Nω-硝基-L-精氨酸甲酯或环氧化酶抑制剂吲哚美辛预处理可减弱BNP在阻力动脉中的冠状动脉舒张作用,而不影响心外膜血管舒张。用ATP敏感性钾通道阻滞剂格列本脲预处理可增强心外膜对BNP的血管舒张反应。我们得出结论,BNP主要在心外膜传导血管中发挥冠状动脉舒张作用。在ET-1预收缩的动脉中,对BNP的血管舒张反应增强。BNP诱导的冠状动脉阻力血管舒张可能部分通过一氧化氮和/或前列腺素释放介导。

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