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Excitation—contraction coupling in the smooth muscle cells of the rabbit main pulmonary artery

机译:激发-收缩在兔主肺动脉平滑肌细胞中的耦合

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摘要

1. Increasing the external K concentration depolarizes the smooth muscle cells of the main pulmonary artery, and this depolarization reaches a maximal slope of 58 mV for a tenfold change of [K]o. The threshold depolarization for inducing contraction is at 4 mV and the maximal contraction is reached at a [K]o of 58 mM.2. Noradrenaline concentrations between 2 × 10-8 M and 10-7 M induce tension without depolarizing the cells, but at higher concentrations noradrenaline not only elicits a large tension response but also depolarizes the cells in a dose-dependent way.3. The effect of noradrenaline on the pulmonary artery is appreciably modified by substituting sucrose for NaCl: the cells are slightly hyperpolarized and the tension response is very much reduced.4. By studying the tension response to noradrenaline in other experimental conditions which cause a small hyperpolarization of the cells, such as 5 mM-[Ca]o, 2.9 mM-[K]o or a small depolarization, such as 11·9 mM-[K]o, it was found that a slight modification of the membrane potential can exert an important effect on the noradrenaline response.5. A simultaneous decrease of [Ca]o and [Na]o reduces the tension response to all noradrenaline concentrations. It was found that a reduction of [Na]o exerts a more depressing effect than a reduction of [Ca]o. In interpreting these results we have to take into account changes of the membrane potential, of availability of Ca, and some competition between external Ca and Na.6. A study of the effect of different concentrations of noradrenaline in Krebs solutions and Ca-free solution has shown that concentrations up to 2·5 × 10-7 M elicit contraction by increasing the Ca influx, while higher concentrations also induce a release of cellular Ca.7. Caffeine depolarizes the cells and reduces the membrane resistance. It modifies the K, Cl and Ca fluxes in the same way as noradrenaline, but it suppresses the mechanical response induced by noradrenaline.
机译:1.增加外部K浓度会使肺主动脉的平滑肌细胞去极化,并且该去极化的最大斜率达到58 mV,这是[K] o十倍变化的原因。诱导收缩的阈值去极化为4 mV,[K] o为58 mM.2时达到最大收缩。在2×10 -8 M和10 -7 M之间的去甲肾上腺素浓度诱导张力而不使细胞去极化,但在更高浓度下,去甲肾上腺素不仅引起大的张力反应,而且去极化细胞呈剂量依赖性3。用蔗糖代替氯化钠可明显改善去甲肾上腺素对肺动脉的作用:细胞略有超极化,张力反应大大降低。4。通过研究在其他实验条件下对去甲肾上腺素的张力反应,这些条件会引起细胞小的超极化,例如5 mM- [Ca] o,2.9 mM- [K] o或小的去极化,例如11·9 mM- [有人发现,膜电位的轻微改变可对去甲肾上腺素反应产生重要影响。5。同时降低[Ca] o和[Na] o可降低对所有去甲肾上腺素浓度的张力反应。已经发现,与[Ca] o的减少相比,[Na] o的减少具有更令人沮丧的效果。在解释这些结果时,我们必须考虑膜电位的变化,Ca的有效性以及外部Ca与Na.6之间的竞争。对不同浓度的去甲肾上腺素在克雷布斯溶液和无钙溶液中的作用的研究表明,高达2·5×10 -7 M的浓度通过增加Ca流入而引起收缩,而更高的浓度也诱导细胞Ca.7的释放。咖啡因可使细胞去极化并降低膜阻力。它以与去甲肾上腺素相同的方式修饰K,Cl和Ca的通量,但抑制了去甲肾上腺素引起的机械响应。

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