Conduction of vasomotor responses in arterioles: a role for cell-to-cell coupling?
Conduction of vasomotor responses in arterioles: a role for cell-to-cell coupling?
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DOI：
10.1152/ajpheart.1989.256.3.h838
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发表时间：
1989-03
期刊：
影响因子：
--
通讯作者：
S. Segal;B. Duling
中科院分区：
文献类型：
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作者：
S. Segal;B. Duling
由乙酰胆碱（ACh）或去甲肾上腺素（NE）的离子电渗应用触发的小动脉的血管反应沿血管壁沿着传导。本实验旨在阐明灌流的颊囊制备在戊巴比妥麻醉仓鼠微动脉的传导机制。局部毒蕈碱或肾上腺素能受体阻断阿托品或酚妥拉明，分别产生的小动脉段，不影响通过该地区的封锁，但没有阻断血管紧张素反应ACh或NE应用于该部分的传播。因此，毒蕈碱和α-肾上腺素能受体可以触发血管反应的传播，但这些受体不参与其传导。河豚毒素不影响局部或传播的ACh或NE的反应。用钙拮抗剂（维拉帕米、地尔硫卓、硝苯地平或锰）治疗小动脉节段引起局部最大扩张，但不影响通过扩张区域的传播。前面的发现反对神经传播途径。去极化溶液（137 mM KCl）应用微量移液器的小动脉节段引起局部和传播性血管收缩和显着衰减ACh诱导的传播性血管舒张（P <0.05）。缝隙连接通讯的假定拮抗剂（高渗蔗糖溶液，辛醇，CO2）可逆地减弱或消除传播的反应。我们假设，血管反应的传播沿着小动脉是通过局部的膜电位的变化继发于受体占领和电位的变化通过缝隙连接耦合平滑肌细胞，内皮细胞，或两者电紧张性传播。
Vasomotor responses of arterioles triggered by the iontophoretic application of acetylcholine (ACh) or norepinephrine (NE) are conducted along the vessel wall. The present experiments focus on elucidating the mechanism of conduction in arterioles of the superfused cheek pouch preparation in pentobarbital-anesthetized hamsters. Localized muscarinic or adrenergic receptor blockade on an arteriolar segment produced by atropine or phentolamine, respectively, did not affect propagation through the region of blockade but did block vasomotor responses to ACh or NE applied to the segment. Thus muscarinic and alpha-adrenergic receptors can trigger the propagation of vasomotor responses, but these receptors are not involved in their conduction. Tetrodotoxin did not affect either local or propagated responses to ACh or NE. Treatment of arteriolar segments with calcium antagonists (verapamil, diltiazem, nifedipine, or manganese) caused maximal dilation locally but did not affect propagation through the dilated region. The preceding findings argue against a neural pathway for propagation. A depolarizing solution (137 mM KCl) applied by micropipette to arteriolar segments caused both local and propagated vasoconstriction and significantly attenuated propagated vasodilation induced with ACh (P less than 0.05). Putative antagonists of gap-junctional communication (hypertonic sucrose solution, octanol, CO2) reversibly attenuated or abolished propagated responses. We hypothesize that propagation of vasomotor responses along arterioles is initiated via a local change in membrane potential secondary to receptor occupation and that changes in potential spread electrotonically through gap junctions coupling smooth muscle cells, endothelial cells, or both.