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内源性和外源性激动剂诱导的大鼠阻力动脉中[Ca2+]i与张力之间偶联的变化。

Endogenous and exogenous agonist-induced changes in the coupling between [Ca2+]i and force in rat resistance arteries.

作者信息

Jensen P E, Mulvany M J, Aalkjaer C

机构信息

Institute of Pharmacology, University of Aarhus, Denmark.

出版信息

Pflugers Arch. 1992 Apr;420(5-6):536-43. doi: 10.1007/BF00374630.

DOI:10.1007/BF00374630
PMID:1614828
Abstract

The relationship between isometric tension and free cytoplasmic calcium, [Ca2+]i, was investigated in rat isolated resistance arteries using fura-2. Depolarisation with 125 mM K+ induced a tonic contraction, while [Ca2+]i increased transiently but stabilised above resting [Ca2+]i. Furthermore, the tension/[Ca2+]i ratio was lower during activation with 125 mM K+ if the effect of endogenous noradrenaline (NA) was inhibited. Concentration/response curves with NA and K+ indicated that NA increased the sensitivity to [Ca2+]i. Calcium concentration/response curves in the presence of 10 microM NA or 125 mM K+ showed that NA could induce force at or below resting [Ca2+]i, while for any given bath calcium concentration, [Ca2+]i was similar in the presence of NA or K+. Addition of NA or vasopressin (AVP) to vessels depolarised with 125 mM K+ caused force development but no increase in [Ca2+]i, suggesting that agonists increase the efficacy of [Ca2+]i. However, during activation with AVP the efficacy of [Ca2+]i decreased time-dependently. The results suggest that in resistance arteries [Ca2+]i plays a crucial role in excitation-contraction coupling, but the tension/[Ca2+]i relationship can be modified by exogenous and endogenous agonists.

摘要

利用fura-2在大鼠离体阻力动脉中研究了等长张力与游离细胞质钙浓度[Ca2+]i之间的关系。用125 mM K+进行去极化诱导了强直性收缩,而[Ca2+]i短暂升高,但在静息[Ca2+]i之上稳定下来。此外,如果内源性去甲肾上腺素(NA)的作用被抑制,在用125 mM K+激活期间,张力/[Ca2+]i比值较低。NA和K+的浓度-反应曲线表明,NA增加了对[Ca2+]i的敏感性。在存在10 microM NA或125 mM K+的情况下的钙浓度-反应曲线表明,NA可以在静息[Ca2+]i或其以下诱导张力,而对于任何给定的浴槽钙浓度,在存在NA或K+的情况下[Ca2+]i相似。向用125 mM K+去极化的血管中添加NA或血管加压素(AVP)会导致张力产生,但[Ca2+]i没有增加,这表明激动剂增加了[Ca2+]i的效力。然而,在用AVP激活期间,[Ca2+]i的效力随时间依赖性降低。结果表明,在阻力动脉中,[Ca2+]i在兴奋-收缩偶联中起关键作用,但张力/[Ca2+]i关系可被外源性和内源性激动剂改变。

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