Khalil R A, van Breemen C
Department of Pharmacology, University of Miami School of Medicine, FL 33136.
Pflugers Arch. 1990 Aug;416(6):727-34. doi: 10.1007/BF00370622.
The changes in isometric force and the underlying fluctuations in intracellular free calcium concentration ([Ca2+]i) were monitored simultaneously in thin sheets of rabbit inferior vena cava loaded with the fluorescent Ca2+ indicator fura-2. In resting tissues bathed in physiological saline solution, the estimated [Ca2+]i was approximately 105 nM. The alpha-adrenergic agonist norepinephrine (10 microM) caused an initial rise in [Ca2+]i to 264 nM during force development, which dropped to 216 nM during force maintenance. The maintained norepinephrine-induced increase in force and [Ca2+]i was reversed in Ca2(+)-free (2 mM EGTA) solution. Membrane depolarization by high K+ (80 mM) significantly increased [Ca2+]i to 234 nM. Compared to norepinephrine, high K+ caused about the same steady-state increase in [Ca2+]i, but a smaller increase in force. [Ca2+]i/force curves were constructed at different concentrations of extracellular Ca2+, with either norepinephrine or high K+ as a stimulant. The curve generated with norepinephrine was located to the left of that generated with high K+.
在加载了荧光钙指示剂fura - 2的兔下腔静脉薄片中,同时监测等长力的变化以及细胞内游离钙浓度([Ca2+]i)潜在的波动情况。在浸泡于生理盐溶液中的静息组织中,估计的[Ca2+]i约为105 nM。α - 肾上腺素能激动剂去甲肾上腺素(10 μM)在力量发展过程中使[Ca2+]i最初升高至264 nM,在力量维持过程中降至216 nM。在无钙(2 mM EGTA)溶液中,去甲肾上腺素诱导的力量和[Ca2+]i的持续增加被逆转。高钾(80 mM)引起的膜去极化使[Ca2+]i显著增加至234 nM。与去甲肾上腺素相比,高钾引起的[Ca2+]i稳态增加大致相同,但力量增加较小。在不同细胞外钙浓度下,以去甲肾上腺素或高钾作为刺激物构建了[Ca2+]i/力量曲线。用去甲肾上腺素生成的曲线位于用高钾生成的曲线左侧。