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Methyl palmitate modulates the nicotine-induced increase in basilar arterial blood flow
Microcirculation ( IF 1.9 ) Pub Date : 2021-02-17 , DOI: 10.1111/micc.12686
Hsu Chun-Kai, Chang Hsi-Hsien, Chang Shang-Jen, Yang Shei-Dei Stephen, Huang Kuo-Feng

Methyl palmitate (MP) is a fatty acid methyl ester. Our recent study indicated that adrenergic nerve-dependent functional sympathetic-sensory nerve interactions were abolished by MP in mesenteric arteries. However, the effect of MP on perivascular nerves and cerebral blood flow remains unclear. In this study, the increase in basilar arterial blood flow (BABF) after the topical application of nicotinic acetylcholine receptor agonists was measured using laser Doppler flowmetry in anesthetized rats. The choline (a selective α7-nicotinic acetylcholine receptor agonist)-induced increase in BABF was abolished by tetrodotoxin (a neurotoxin), NG-nitro-L-arginine (a nonselective NO synthase inhibitor), α-bungarotoxin (a selective α7-nicotinic acetylcholine receptor inhibitor), and chronic sympathetic denervation. In addition, the nicotine (a nicotinic acetylcholine receptor agonist)-induced increase in BABF was inhibited by MP in a concentration-dependent manner. The acetylcholine-induced increase in BABF was not affected by MP. The myography results revealed that nicotine-induced vasorelaxation was significantly inhibited by MP, but was reversed by chelerythrine (a protein kinase C inhibitor). MP-induced vasodilation was significantly greater in BA rings without endothelium compared to those with endothelium. Meanwhile, MP did not affect baseline BABF. Our results indicate that MP acts as a neuromodulator in the cerebral circulation where it activates the PKC pathway and causes a diminished nicotine-induced increase in blood flow in the brainstem, and that the vasorelaxation effect of MP may play a minor role.

中文翻译:

棕榈酸甲酯调节尼古丁诱导的基底动脉血流量增加

棕榈酸甲酯 (MP) 是一种脂肪酸甲酯。我们最近的研究表明,肠系膜动脉中的 MP 消除了依赖于肾上腺素能神经的功能性交感 - 感觉神经相互作用。然而,MP对血管周围神经和脑血流的影响仍不清楚。在这项研究中,使用激光多普勒血流仪在麻醉大鼠中测量局部应用​​烟碱型乙酰胆碱受体激动剂后基底动脉血流量 (BABF) 的增加。胆碱(一种选择性α7-烟碱乙酰胆碱受体激动剂)诱导的 BABF 增加被河豚毒素(一种神经毒素)消除,NG-硝基-L-精氨酸(一种非选择性 NO 合酶抑制剂)、α-银环蛇毒素(一种选择性 α7-烟碱乙酰胆碱受体抑制剂)和慢性交感神经去神经支配。此外,烟碱(烟碱型乙酰胆碱受体激动剂)诱导的 BABF 增加被 MP 以浓度依赖性方式抑制。乙酰胆碱诱导的 BABF 增加不受 MP 的影响。肌电图结果显示尼古丁诱导的血管舒张被 MP 显着抑制,但被白屈菜红碱(一种蛋白激酶 C 抑制剂)逆转。与有内皮的 BA 环相比,MP 诱导的血管舒张在没有内皮的 BA 环中显着更大。同时,MP 不影响基线 BABF。
更新日期:2021-02-17
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