Nitric oxide, ACh, and electrical and mechanical properties of canine arterial smooth muscle.
Nitric oxide, ACh, and electrical and mechanical properties of canine arterial smooth muscle.
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一氧化氮、乙酰胆碱以及犬动脉平滑肌的电学和机械特性。
DOI：
10.1152/ajpheart.1988.255.1.h207
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
--
作者：
Komori,K;Lorenz,RR;Vanhoutte,PM
本文研究了一氧化氮和乙酰胆碱（ACh）对犬肠系膜动脉平滑肌细胞电特性和力学特性的影响。用前列腺素F2 α收缩有或无内皮的分离组织。一氧化氮引起的浓度依赖性松弛环与无内皮。ACh仅在有内皮的动脉中引起浓度依赖性舒张。对一氧化氮和乙酰胆碱的舒张作用可被亚甲蓝或氧合血红蛋白所抑制。无论是否存在前列腺素F2 α，ACh引起血管平滑肌细胞膜的短暂超极化。机械去除内皮细胞或阿托品处理后，没有观察到乙酰胆碱诱导的短暂超极化。一氧化氮（小于或等于8 × 10（-6）M）不改变膜电位，无论是否存在内皮。血管周围神经刺激产生的兴奋性接头电位被ACh抑制，但不被一氧化氮抑制。这些结果表明，在犬肠系膜动脉中，1）ACh产生的内皮源性超极化因子不是一氧化氮; 2）一氧化氮通过直接作用松弛血管平滑肌; 3）一氧化氮不改变肾上腺素能神经传递。
The effects of nitric oxide and acetylcholine (ACh) were investigated on the electrical and mechanical properties of vascular smooth muscle cells of the canine mesenteric artery. Isolated tissues with or without the endothelium were contracted with prostaglandin F2 alpha. Nitric oxide caused comparable concentration-dependent relaxations in rings with and without endothelium. ACh induced concentration-dependent relaxations only in arteries with endothelium. The relaxations to both nitric oxide and ACh were inhibited by methylene blue or oxyhemoglobin. Either in the presence or absence of prostaglandin F2 alpha, ACh caused transient hyperpolarization of the cell membrane of the vascular smooth muscle. The ACh-induced transient hyperpolarization was not observed after mechanical removal of the endothelial cells or after treatment with atropine. Nitric oxide (less than or equal to 8 X 10(-6) M) did not alter membrane potential, in either the presence or absence of the endothelium. The excitatory junction potentials generated by perivascular nerve stimulation were inhibited by ACh but not by nitric oxide. These results suggest that in the canine mesenteric artery 1) the endothelium-derived hyperpolarizing factor generated by ACh is not nitric oxide; 2) nitric oxide relaxes vascular smooth muscle by a direct effect; and 3) nitric oxide does not modify adrenergic neurotransmission.