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牛气管平滑肌中的钙动员与等长张力:沙丁胺醇和组胺的作用

Calcium mobilization and isometric tension in bovine tracheal smooth muscle: effects of salbutamol and histamine.

作者信息

Hirsh A J, Benishin C G, Jones R L, Pang P K, Man S F

机构信息

Department of Physiology, University of Alberta, Edmonton, Canada.

出版信息

Cell Calcium. 1996 Jan;19(1):73-81. doi: 10.1016/s0143-4160(96)90014-7.

Abstract

We determined if decreases in relative free intracellular calcium concentration ([Ca2+]i) caused by salbutamol, a selective beta2-adrenoreceptor agonist, were paralleled by calcium egression from the cytosol in bovine trachealis muscle strips. [Ca2+]i, or tissue-surface extracellular calcium changes (Ts[Ca2+]ext), were monitored using Fluo-3 acetoxymethylester or Fluo-3 pentaammonium salt simultaneously with isometric tension. Salbutamol (1 microM) decreased histamine-induced isometric tension from an average peak tension of 128.5 +/- 18.4 to -4.9 +/- 0.3 mN/mm2, and reduced the associated sustained increases in [Ca2+]i from 100% at peak to 20.4 +/- 7.6%. Both histamine-induced elevation in [Ca2+]i and isometric tension were reversed completely by forskolin (1 microM). In muscle strip at active resting tension, salbutamol caused a decrease (49.6 +/- 12.1%) in [Ca2+]i. Following precontraction with histamine, salbutamol caused an immediate and sustained increase in Ts[Ca2+]ext which was not seen in a Na(+)-free solution. Finally, propranolol (10 microM) blocked both increases in Ts[Ca2+]ext and muscle relaxation caused by salbutamol. These findings indicate that in bovine trachealis muscle, the effect of salbutamol to decrease [Ca2+]i and isometric tension is via a beta2-adrenoceptor, and the changes in [Ca2+]i are by an increase in calcium egression via the Na(+)/Ca2+ exchanger, and reuptake by myoplasmic stores.

摘要

我们研究了选择性β2肾上腺素能受体激动剂沙丁胺醇引起的细胞内相对游离钙浓度([Ca2+]i)降低是否与牛气管肌条中钙离子从胞质溶胶的流出相平行。使用Fluo-3乙酰氧甲酯或Fluo-3五铵盐同时监测[Ca2+]i或组织表面细胞外钙变化(Ts[Ca2+]ext)与等长张力。沙丁胺醇(1μM)将组胺诱导的等长张力从平均峰值张力128.5±18.4降低至-4.9±0.3 mN/mm2,并将相关的[Ca2+]i持续升高从峰值时的100%降低至20.4±7.6%。组胺诱导的[Ca2+]i升高和等长张力均被福斯可林(1μM)完全逆转。在处于主动静息张力的肌条中,沙丁胺醇导致[Ca2+]i降低(49.6±12.1%)。在用组胺预收缩后,沙丁胺醇导致Ts[Ca2+]ext立即且持续升高,而在无钠溶液中未观察到这种情况。最后,普萘洛尔(10μM)阻断了沙丁胺醇引起的Ts[Ca2+]ext升高和肌肉松弛。这些发现表明,在牛气管肌中,沙丁胺醇降低[Ca2+]i和等长张力的作用是通过β2肾上腺素能受体介导的,[Ca2+]i的变化是由于通过Na+/Ca2+交换器的钙流出增加以及肌浆网的再摄取。

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