Role of endothelium-derived relaxing factor in parasympathetic coronary vasodilation.

Role of endothelium-derived relaxing factor in parasympathetic coronary vasodilation.
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内皮衍生舒张因子在副交感冠状血管舒张中的作用。

DOI:
10.1152/ajpheart.1992.262.5.h1579
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发表时间:
1992
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Feigl,EO
Feigl,EO
中科院分区:
--
文献类型:
--
作者:
Broten,TP;Miyashiro,JK;Moncada,S;Feigl,EO

文献摘要

被引文献

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乙酰胆碱输注后血管舒张是由于内皮源性舒张因子(EDRF)的释放。然而,EDRF在神经源性冠状血管舒张中的作用,当乙酰胆碱在血管外膜-中膜连接处释放时,尚未确定。在本研究中,使用EDRF合成的特异性抑制剂,硝基-L-精氨酸甲酯(L-NAME),EDRF在副交感冠状血管舒张中的作用进行了测试。实验在闭胸、α-氯醛糖麻醉的狗上进行,心脏以恒定速率起搏。服用酚妥拉明和普萘洛尔来阻断α和β肾上腺素能受体,服用布洛芬来抑制前列腺素合成。冠状动脉内灌注L-NAME可降低冠状动脉内乙酰胆碱或迷走神经刺激引起的血管舒张反应。冠状动脉对内皮非依赖性血管扩张剂硝酸甘油的反应不受L-NAME的影响。这些数据表明,L-NAME特异性抑制由乙酰胆碱和迷走神经刺激引起的冠状动脉血管舒张,表明副交感神经冠状动脉血管舒张依赖于EDRF。
Vasodilation following the infusion of acetylcholine is due to the release of endothelium-derived relaxing factor (EDRF). However, the role of EDRF in neurogenic coronary vasodilation, when acetylcholine is released outside the vessel at the adventitial-medial junction, has not been established. The action of EDRF in parasympathetic coronary vasodilation was tested in the present study using a specific inhibitor of EDRF synthesis, nitro-L-arginine methyl ester (L-NAME). Experiments were conducted on closed-chest, alpha-chloralose-anesthetized dogs with the heart paced at a constant rate. Phentolamine and propranolol were administered to block alpha- and beta-adrenergic receptors, and ibuprofen was given to inhibit prostaglandin synthesis. Intracoronary infusion of L-NAME decreased the coronary vasodilation in response to intracoronary acetylcholine or vagal stimulation. The coronary response to the endothelium-independent vasodilator nitroglycerin was unaffected by L-NAME. These data demonstrate that L-NAME specifically inhibits coronary vasodilation caused by acetylcholine and vagal stimulation, indicating that parasympathetic coronary vasodilation is dependent on EDRF.