Differential effects of carbachol on cytosolic calcium levels in vascular endothelium and smooth muscle.
Differential effects of carbachol on cytosolic calcium levels in vascular endothelium and smooth muscle.
复制标题
卡巴胆碱对血管内皮和平滑肌细胞质钙水平的不同影响。
DOI：
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发表时间：
1990
影响因子：
3.5
通讯作者：
H. Karaki
中科院分区：
文献类型：
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作者：
K. Sato;H. Ozaki;H. Karaki
观察去甲肾上腺素(NE)、卡巴胆碱(CCH)和组胺(His)对大鼠血管张力及血管内皮细胞和平滑肌细胞胞浆C++浓度([Ca++]i)的影响。在内皮细胞表面检测到内皮细胞和平滑肌细胞发出的Fura-2-Ca++荧光。在有内皮的主动脉中，去甲肾上腺素使[Ca++]i和肌张力均升高，而CCH使肌条轻度松弛，使[Ca++]i升高，维拉帕米部分抑制CCH刺激的[Ca++]i。在去甲肾上腺素(NE)刺激的主动脉中加入CCH，肌肉松弛，[Ca++]i增加，且[Ca++]i增加与松弛呈正相关。在无内皮的主动脉中，去甲肾上腺素使[Ca++]i和张力均升高，而CCH无此作用。当仅从检测到Fura-2-Ca++荧光的一小块区域去除内皮时，CCH松弛肌肉而不改变[Ca++]i。在这种准备中，NE增加了[Ca++]i和肌张力，连续加入CCH使肌肉松弛，但[Ca++]i略有下降，提示收缩元件对[Ca++]i的敏感性降低。在无Ca~(++)溶液中，CCH仅在有内皮细胞存在的情况下才引起[Ca~(++)]i的一过性升高和肌张力的降低。他的作用与CCH相似。而硝普钠则使去甲肾上腺素(NE)刺激的有或无内皮血管[Ca++]i降低，肌肉松弛。这些结果提示，CCH和His可使内皮细胞内[Ca++]i升高，从而调节内皮源性松弛因子的合成和/或释放。内皮源性松弛因子可降低血管内皮细胞内[Ca++]i，降低收缩因子对钙离子的敏感性，从而起到扩张血管的作用。
Effects of norepinephrine (NE), carbachol (CCh) and histamine (HIS) on vascular tone and the endothelial and smooth muscle cytosolic C++ levels ([Ca++]i) were examined in rat aorta. The fura-2-Ca++ fluorescence emitted from endothelial and smooth muscle cells was detected at the endothelial surface. In the aorta with endothelium, NE increased both [Ca++]i and muscle tension whereas CCh slightly relaxed the muscle and increased [Ca++]i. The CCh-stimulated [Ca++]i was partially inhibited by verapamil. Addition of CCh to the NE-stimulated aorta relaxed the muscle with additional increase in [Ca++]i and positive correlation was obtained between the increase in [Ca++]i and relaxation. In the aorta without endothelium, NE increased both [Ca++]i and tension although CCh was ineffective. When endothelium was removed only from a small area from where the fura-2-Ca++ fluorescence was detected, CCh relaxed the muscle without changing [Ca++]i. In this preparation, NE increased both [Ca++]i and muscle tension and sequential addition of CCh relaxed the muscle with a small decrease in [Ca++]i, suggesting that Ca++ sensitivity of contractile elements is decreased. In Ca+(+)-free solution, CCh induced a transient increase in [Ca++]i and a decrease in muscle tension only in the presence of endothelium. HIS showed similar effects as CCh. By contrast, sodium nitroprusside decreased [Ca++]i and relaxed the muscle in NE-stimulated aorta with or without endothelium. These results suggest that CCh and HIS increase [Ca++]i in the endothelial cells which regulates the synthesis and/or release of endothelium-derived relaxing factor. Endothelium-derived relaxing factor may decrease [Ca++]i in the smooth muscle cells and also decrease Ca++ sensitivity of contractile elements resulting in vasodilatation.