THE CORONARY VASODILATOR EFFECT OF NEUROTENSIN IN THE GUINEA-PIG ISOLATED HEART
THE CORONARY VASODILATOR EFFECT OF NEUROTENSIN IN THE GUINEA-PIG ISOLATED HEART
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DOI：
10.1016/0196-9781(86)90010-0
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发表时间：
1986-05-01
期刊：
影响因子：
3
通讯作者：
RIOUX, F
中科院分区：
文献类型：
--
作者：
BACHELARD, H;STPIERRE, S;RIOUX, F
将神经降压素（NT）注入豚鼠离体电驱动心脏，引起心肌灌注压的浓度依赖性降低，伴随着心肌张力的成比例增加。由NT引起的心肌灌注压的降低（归因于NT的冠状血管扩张作用）高度依赖于灌注压的基础（NT输注前）水平，在高灌注压下更大（例如，75 mmHg）的值比在较低的值（例如，50和25 mmHg）。新斯的明和阿托品分别增强和抑制NT的灌注压降低作用。麦角新碱对该作用有轻微抑制作用。然而，它不受普萘洛尔，吲哚美辛或苯海拉明和西咪替丁的混合物。NT引起的心肌灌注压降低可被NT受体脱敏所消除，而对乙酰胆碱或血管活性肠肽（VIP）引起的心肌灌注压降低的影响最小。这些结果表明NT在豚鼠冠状血管中具有扩张血管的作用。这种作用可能涉及从NT刺激的心脏胆碱能（迷走神经）神经元和/或神经末梢释放的乙酰胆碱的参与，并由特异性NT受体介导。心内5-羟色胺和/或其受体对NT的冠状血管舒张作用的可能贡献进行了讨论。
Neurotensin (NT) infusions into isolated, electrically-driven hearts of guinea pigs, elicited concentration-dependent reductions of myocardial perfusion pressure accompanied by proportional increases of myocardial tension. The decrease of myocardial perfusion pressure caused by NT (attributed to the coronary vasodilator effect of NT) was highly dependent on basal (pre-NT infusions) levels of perfusion pressure, being larger at high perfusion pressure (e.g., 75 mmHg) values than at lower ones (e.g., 50 and 25 mmHg). The perfusion pressure-lowering effect on NT was potentiated and inhibited by neostigmine and atropine, respectively. It was slightly inhibited by methysergide. However, it was not affected by propranolol, indomethacin or a mixture of diphenhydramine and cimetidine. The decreases of myocardial perfusion pressure caused by NT were abolished by NT receptor desensitization, while those evoked by acetylcholine or vasoactive intestinal peptide (VIP) were minimally affected by the desensitization. These results indicate that NT exerts a vasodilator effect in guinea pig coronary vessels. This effect is likely to involve the participation of acetylcholine released from NT-stimulated cardiac cholinergic (vagal) neurons and/or nerve terminals and to be mediated by specific NT receptors. The possible contribution of intracardiac serotonin and/or its receptors to the coronary vasodilator effect of NT is discussed.