Hayashi M, Aizawa Y, Satoh M, Suzuki K, Shibata A
Jpn Heart J. 1986 Mar;27(2):251-7. doi: 10.1536/ihj.27.251.
The coronary vasoconstrictor effects of neuropeptide Y (NPY) were confirmed in anesthetized closed-chest dogs. This NPY-induced vasoconstriction was not affected by alpha- or beta-adrenergic blockers and nifedipine given into the perfusion circuit abolished the constriction. After intracoronary nifedipine administration, coronary flow exceeded the control level within 60 sec, then returned to a level between the control value before NPY and the lowest value elicited by NPY after 10 min. When nifedipine was given systemically before NPY, the peak response to NPY was attenuated, suggesting a preventive effect of nifedipine on the NPY-induced coronary vasoconstriction. Since NPY is found in the hearts of many species, including man, NPY may cause coronary vasospasms. An effect on NPY-induced coronary vasoconstriction of nifedipine may be compatible with the beneficial clinical effects of this drug.
在麻醉的开胸犬身上证实了神经肽Y（NPY）的冠状动脉收缩作用。这种由NPY诱导的血管收缩不受灌注回路中给予的α或β肾上腺素能阻滞剂的影响，而硝苯地平可消除这种收缩。冠状动脉内给予硝苯地平后，冠状动脉血流在60秒内超过对照水平，然后在10分钟后恢复到NPY给药前对照值与NPY引起的最低值之间的水平。当在给予NPY之前全身给予硝苯地平时，对NPY的峰值反应减弱，提示硝苯地平对NPY诱导的冠状动脉收缩有预防作用。由于在包括人类在内的许多物种的心脏中都发现了NPY，NPY可能会导致冠状动脉痉挛。硝苯地平对NPY诱导的冠状动脉收缩的作用可能与其临床有益效果相符。
