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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Regulation of vascular tone by endothelium-derived hyperpolarizing factor.
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Regulation of vascular tone by endothelium-derived hyperpolarizing factor.

机译：内皮细胞超极化因子对血管张力的调节。

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1. Endothelium-derived hyperpolarizing factor (EDHF) mediates the nitric oxide (NO)-independent component of the relaxation in rat mesenteric arteries. The relationship between hyperpolarization and vascular tone was studied by simultaneous recording of membrane potential with intracellular microelectrodes and tension in ring segments of rat mesenteric arteries. 2. By depolarizing arteries with high potassium solutions, it was determined that the threshold for contraction is approximately -46 mV. Maximum contraction was attained when the arteries were depolarized to -20 mV. Thus, 1 mV depolarization resulted in an approximate 4% increase in tone. This relationship was not altered in spontaneously hypertensive rats. 3. Noradrenaline (0.3 mumol/L) caused contraction and depolarized arteries by 13 mV. Acetylcholine caused endothelium-dependent relaxation and hyperpolarization up to 14 mV. In the presence of N omega-nitro-L-arginine, the EDHF-mediated relaxation was correlated to hyperpolarization. A hyperpolarization of 1 mV corresponded to a 4.3% decrease of the induced tone. 4. At concentrations (10 mumol/L) causing total relaxation, the maximum hyperpolarization induced by NO was only 7.6 mV. 5. A maximum relaxation of 88% was observed with pinacidil (3 mumol/L), despite a 25 mV hyperpolarization. Relaxations to NO and pinacidil were not correlated with hyperpolarization. At similar levels of hyperpolarization, NO and pinacidil elicited more relaxation than EDHF. 6. These studies show that vascular tone is very sensitive to membrane potential change in the range between -46 and -20 mV in the rat mesenteric artery. The relaxation response to EDHF, unlike that to NO and pinacidil, can be accounted for solely by its effect on the membrane potential.
机译：1.内皮源性超极化因子（EDHF）介导大鼠肠系膜动脉舒张反应的一氧化氮（NO）非依赖性成分。通过同时记录细胞内微电极的膜电位和大鼠肠系膜动脉环段张力来研究超极化与血管紧张度之间的关系。 2.通过用高钾溶液使动脉去极化，可以确定收缩的阈值约为-46 mV。当动脉去极化至-20 mV时，可达到最大收缩。因此，1 mV的去极化导致音调增加大约4％。这种关系在自发性高血压大鼠中没有改变。 3.去甲肾上腺素（0.3μmol/ L）引起的收缩和动脉去极化13 mV。乙酰胆碱引起内皮依赖性舒张和超极化，最高达14 mV。在Nω-硝基-L-精氨酸存在下，EDHF介导的弛豫与超极化相关。 1 mV的超极化对应于感应音调降低4.3％。 4.在引起完全弛豫的浓度（10μmol/ L）下，NO诱导的最大超极化仅为7.6 mV。 5.尽管有25 mV的超极化作用，但使用吡那地尔（3μmol/ L）观察到最大松弛为88％。 NO和吡那地尔的松弛与超极化无关。在类似的超极化水平下，NO和频那地尔比EDHF引起更多的松弛。 6.这些研究表明，在大鼠肠系膜动脉中，血管紧张度对膜电位变化非常敏感，范围在-46至-20 mV之间。 EDNO的弛豫响应与NO和频那地尔不同，可以仅通过其对膜电位的影响来解释。

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