豚鼠冠状动脉中M3受体刺激引发内皮源性超极化因子（EDHF）的释放。
Release of endothelium-derived hyperpolarizing factor (EDHF) by M3 receptor stimulation in guinea-pig coronary artery.
作者信息
Hammarström A K, Parkington H C, Coleman H A
机构信息
Department of Physiology, Monash University, Clayton, Victoria, Australia.
出版信息
Br J Pharmacol. 1995 Jul;115(5):717-22. doi: 10.1111/j.1476-5381.1995.tb14992.x.
Abstract
- The muscarinic receptor subtype(s) involved in the release of endothelium-derived hyperpolarizing factor (EDHF) were studied in the guinea-pig coronary artery by recording the membrane potential in the smooth muscle cells with intracellular microelectrodes. 2. Acetylcholine (ACh, pD2 6.68) was 10 times more potent than the M2 agonist, oxotremorine (pD2 5.65) and 500 fold more potent than the M1 agonist, McN-A-343 (pD2 3.95) in evoking the EDHF hyperpolarization. 3. The M3 muscarinic antagonist, 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) was the most potent (pA2 9.5) in inhibiting the release of EDHF evoked by ACh, being more potent than pirenzepine (pA2 6.7), and AFDX-116 (pA2 6.1) which preferentially block M1 and M2 receptors, respectively. 4. These results suggest that EDHF is released from the endothelium of the guinea-pig coronary artery upon the activation of the muscarinic M3 receptor subtype.
摘要
- 通过使用细胞内微电极记录平滑肌细胞的膜电位，研究了豚鼠冠状动脉中参与内皮衍生超极化因子（EDHF）释放的毒蕈碱受体亚型。2. 乙酰胆碱（ACh，pD2 6.68）在诱发EDHF超极化方面的效力比M2激动剂氧化震颤素（pD2 5.65）强10倍，比M1激动剂 McN-A-343（pD2 3.95）强500倍。3. M3毒蕈碱拮抗剂4-二苯基乙酰氧基-N-甲基哌啶甲碘化物（4-DAMP）在抑制ACh诱发的EDHF释放方面效力最强（pA2 9.5），比分别优先阻断M1和M2受体的哌仑西平（pA2 6.7）和AFDX-116（pA2 6.1）更有效。4. 这些结果表明，豚鼠冠状动脉内皮在毒蕈碱M3受体亚型激活后释放EDHF。
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