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犬和猴离体脑动脉对血管舒张神经刺激反应的潜在机制。

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries.

作者信息

Toda N, Okamura T

机构信息

Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.

出版信息

Am J Physiol. 1990 Nov;259(5 Pt 2):H1511-7. doi: 10.1152/ajpheart.1990.259.5.H1511.

DOI:10.1152/ajpheart.1990.259.5.H1511
PMID:1700632
Abstract

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

摘要

从狗和日本猕猴获取的脑动脉条对跨壁电刺激和尼古丁的舒张反应分别被河豚毒素和六甲铵消除,且被一氧化氮(NO)合成抑制剂NG-单甲基-L-精氨酸(L-NMMA)处理所抑制。L-精氨酸可预防并逆转该抑制作用,而D-精氨酸则不能。L-NMMA抑制的舒张反应不会因外源性应用NO而增强。内皮剥脱并未改变对跨壁刺激和尼古丁的反应或L-NMMA的抑制作用。D-NMMA不会抑制对血管舒张神经刺激的反应。狗冠状动脉由跨壁刺激引起的舒张反应不会被L-NMMA抑制,但会被普萘洛尔逆转至收缩反应。用吲哚美辛处理的狗脑动脉由P物质引起的舒张反应依赖于内皮且被L-NMMA抑制,而由NO和硝酸甘油引起的非内皮依赖性舒张反应则不受影响。结论是,血管舒张神经的化学和电刺激使狗和猴的脑动脉舒张,可能是通过NO介导,而非NO对血管舒张递质释放的刺激作用。狗脑动脉由P物质引起的内皮依赖性舒张反应似乎是由NO介导的。

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