CALCIUM-FORCE RELATIONSHIPS AS DETECTED WITH AEQUORIN IN 2 DIFFERENT VASCULAR SMOOTH MUSCLES OF THE FERRET
CALCIUM-FORCE RELATIONSHIPS AS DETECTED WITH AEQUORIN IN 2 DIFFERENT VASCULAR SMOOTH MUSCLES OF THE FERRET
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DOI：
10.1113/jphysiol.1985.sp015900
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发表时间：
1985-01-01
影响因子：
5.5
通讯作者：
MORGAN, KG
中科院分区：
文献类型：
--
作者：
DEFEO, TT;MORGAN, KG
1. 用化学方法将生物发光钙指示剂黄钙素装入离体雪貂门静脉和雪貂主动脉。Aequorin光发射（[Ca2+]i的函数）与张力同时记录。2. 假设[Mg2+]i为0.5 mM， [Ca2+]i为1.8倍。10-7 M在未刺激的门静脉22度处。C，静息音可以忽略不计。相反，在未刺激的主动脉22度。C有明显的基底张力，[Ca2+]i为2.7倍。10-7米。在门静脉和主动脉中，钾去极化引起细胞内Ca2+的单相上升与张力的上升平行，而苯肾上腺素在力发展期间引起最初的光峰值，然后在力维持期间下降到一个更低的平台水平。4. 当细胞内[Ca2+]通过增加钾去极化程度或减少细胞外[Ca2+]而发生变化时，通过绘制校准的aequorin光与力的关系来生成钙-力曲线。5. 在门静脉和主动脉均有去极化钾存在时，稳态钙力曲线在苯肾上腺素存在时向左移动。6. 主动脉钙-力关系呈逆时针迟滞。相反，在门静脉中没有明显的迟滞，这表明在苯肾上腺素存在下，收缩器官钙敏感性的明显变化一定是由钙以外的第二信使引起的。
1. The bioluminescent calcium indicator aequorin was chemically loaded into isolated strips of ferret portal vein and ferret aorta. Aequorin light emission (a function of [Ca2+]i) was recorded simultaneously with tension. 2. Assuming an [Mg2+]i of 0.5 mM, [Ca2+]i was 1.8 .times. 10-7 M in the unstimulated portal vein at 22.degree. C where there was negligible resting tone. In contrast, in the unstimulated aorta at 22.degree. C where there was significant basal tone, the [Ca2+]i was 2.7 .times. 10-7 M. 3. In both portal vein and aorta, potassium depolarization caused a monophasic rise in intracellular Ca2+ in parallel with the rise in tension, whereas phenylephrine caused an initial spike of light during the period of the force development which then fell to a much lower plateau level during the period of force maintenance. 4. Calcium-force curves were generated by plotting calibrated aequorin light against force while intracellular [Ca2+] was made to change either by increasing degrees of potassium depolarization or decreasing extracellular [Ca2+]. 5. The steady-state calcium-force curve in the presence of phenylephrine was shifted to the left of the curve in the presence of potassium depolarization in both the portal vein and aorta. 6. In the aorta there was a counter-clockwise hysteresis in the calcium-force relationship. In contrast, in the portal vein there was no demonstrable hysteresis, indicating that the apparent change in calcium sensitivity of the contractile apparatus in the presence of phenylephrine must be caused by a second messenger other than calcium.