Cholinergic mechanism in the large cat cerebral artery.
Cholinergic mechanism in the large cat cerebral artery.
复制标题
大型猫脑动脉的胆碱能机制。
DOI：
10.1161/01.res.50.6.870
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发表时间：
1982
影响因子：
20.1
通讯作者：
Lee,TJ
中科院分区：
文献类型：
--
作者：
Lee,TJ
本实验采用离体猫脑动脉（基底动脉、大脑中动脉、大脑前动脉和颈内动脉）进行研究。低浓度（3 × 10（-8）至3 × 10（-6）M）的ACh诱导舒张，而高浓度（10（-5）至3 × 10（-3）M）的ACh诱导血管内皮细胞收缩。相比之下，任何浓度（10（-6）至3 × 10（-3）M）仅在无内皮的动脉中诱导收缩。阿托品（3 × 10（-6）至3 × 10（-5）M）阻断ACh诱导的舒张和收缩，毒扁豆碱（3 × 10（-6）M）增强ACh诱导的舒张和收缩。这些结果表明，由外源性ACh引起的舒张是完全依赖于内皮细胞和ACh对平滑肌细胞的直接作用的主要效果是收缩。神经刺激（TNS）在有或无内皮的动脉中引起频率依赖性舒张。阿托品和毒扁豆碱均不影响TNS诱导的扩张反应。这与血管壁中神经和内皮细胞之间的广泛分离一起表明ACh不参与TNS诱导的血管舒张。此外，在任何频率下，在无内皮细胞的动脉中，TNS诱导的舒张不是小于而是大于有内皮细胞的动脉。河豚毒素（TTX）或冷藏去神经阻断TNS诱导的血管舒张并不能阻止动脉对ACh或乙酰甲胆碱（MCh）的反应。提示TNS引起的血管舒张作用不依赖于内皮细胞，是由于一种尚待鉴定的扩张递质对平滑肌细胞的直接作用。本研究的结果支持了我们以前的发现，在猫的大脑动脉。ACh更可能是缩窄性递质而不是扩张性递质。
The isolated cat cerebral arteries (basilar, middle cerebral, anterior cerebral, and internal carotid) were studied in vitro. ACh at low concentration (3 x 10(-8) to 3 x 10(-6) M) induced relaxation, and at high concentration (10(-5) to 3 x 10(-3) M) induced constriction of the arteries with endothelial cells. In contrast, concentration of any magnitude (10(-6) to 3 x 10(-3) M) induced constriction exclusively in arteries without endothelium. Atropine (3 x 10(-6) to 3 x 10(-5) M) blocked and physostigmine (3 x 10(-6) M) potentiated both ACh-induced relaxation and constriction. These results suggest that the relaxation induced by exogenous ACh is solely dependent on the endothelial cells and that the primary effect of the direct action of ACh on the smooth muscle cells is constriction. Transmural nerve stimulation (TNS) induced a frequency-dependent relaxation in the arteries with or without endothelium. Neither atropine nor physostigmine affected the TNS-induced dilator response in either preparation. This, together with the wide separation between the nerve and endothelium in the vessel wall, suggests that ACh is not involved in TNS-induced vasodilation. Furthermore, the TNS-induced relaxation at any frequency is not smaller but greater in the arteries without endothelial cells than in those with endothelial cells. Blockade of the TNS-induced vasodilation by tetrodotoxin (TTX) or cold storage denervation did not prevent the arteries from relaxing in response to ACh or methacholine (MCh). It is suggested that the TNS-induced vasodilation is independent of the endothelial cells and that the vasodilation is due to the direct action of a yet-to-be identified dilator transmitter on the smooth muscle cells. Results of the present study support our previous finding that, in the cat cerebral artery. ACh is more likely to be a constrictor transmitter than a dilator transmitter.