Endothelial and smooth muscle cell conduction in arterioles controlling blood flow.

Endothelial and smooth muscle cell conduction in arterioles controlling blood flow.
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DOI:
10.1152/ajpheart.1998.274.1.h178
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发表时间:
1998
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
D. Welsh;S. Segal
D. Welsh;S. Segal
中科院分区:
其他
文献类型:
--
作者:
D. Welsh;S. Segal

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用荧光黄染料显微注射法进行细胞内记录,研究了63只金黄地鼠颊囊供血小动脉(直径47 ± 1 μm,n = 63)沿血管壁沿着收缩和扩张的细胞通路。静息状态下,内皮细胞膜电位(-36 ± 1 mV)与平滑肌细胞膜电位(-35 ± 1 mV)无明显差异。微量注射去甲肾上腺素(NE)或苯肾上腺素(PE)可引起平滑肌细胞去极化(5-41 mV)和血管收缩(7-49 μm),但对内皮细胞的E m无影响。KCl在内皮细胞和平滑肌细胞中产生具有相似电动力学的去极化和血管收缩传导。乙酰胆碱触发沿着两个细胞层的血管舒张(2-25 μm)和超极化(3-33 mV)传导;在平滑肌中,这种E m的变化延长,随后是短暂的去极化。这些细胞特异性电生理记录独特地说明去极化和收缩是沿着沿着启动和进行的,不依赖于内皮。此外,血管舒张的传导可以通过超极化沿着同源偶联的内皮细胞和平滑肌细胞的传播来解释,并且细胞层之间具有独特的反应。沿着同源偶联的内皮细胞和平滑肌细胞的超极化传播。内皮和平滑肌之间的不连续性表明这些各自的通路在血流控制期间没有电耦合。
We performed intracellular recording with Lucifer yellow dye microinjection to investigate the cellular pathway(s) by which constriction and dilation are conducted along the wall of arterioles (diameter 47 ± 1 μm, n = 63) supplying blood flow to the cheek pouch of anesthetized hamsters. At rest, membrane potential ( E m) of endothelial (-36 ± 1 mV) and smooth muscle (-35 ± 1 mV) cells was not different. Micropipette delivery of norepinephrine (NE) or phenylephrine (PE) produced smooth muscle cell depolarization (5-41 mV) and vasoconstriction (7-49 μm) at the site of release and along the arteriole with no effect on E m of endothelial cells. KCl produced conduction of depolarization and vasoconstriction with similar electrical kinetics in endothelial and smooth muscle cells. Acetylcholine triggered conduction of vasodilation (2-25 μm) and hyperpolarization (3-33 mV) along both cell layers; in smooth muscle, this change in E m was prolonged and followed by a transient depolarization. These cell-specific electrophysiological recordings uniquely illustrate that depolarization and constriction are initiated and conducted along smooth muscle, independent of the endothelium. Furthermore, conduction of vasodilation is explained by the spread of hyperpolarization along homologously coupled endothelial and smooth muscle cells, with distinctive responses between cell layers. The discontinuity between endothelium and smooth muscle indicates that these respective pathways are not electrically coupled during blood flow control.