Increased intracellular Na+ augments mobilization of Ca2+ from SR in vascular smooth muscle cells.
Increased intracellular Na+ augments mobilization of Ca2+ from SR in vascular smooth muscle cells.
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细胞内 Na 的增加增强了血管平滑肌细胞中 SR 中 Ca2 的动员。
DOI：
10.1152/ajpcell.1994.266.1.c311
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Blaustein,MP
中科院分区：
文献类型：
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作者：
Borin,ML;Tribe,RM;Blaustein,MP
在A7 r5系血管平滑肌细胞中研究了细胞内Na+浓度（[Na+]cyt）升高对细胞内钙库中Ca 2+量的影响。通过肌浆网（SR）释放Ca 2+引起的胞浆游离Ca 2+浓度（[Ca 2 +]cyt）的升高来估计Fura 2负载细胞中储存的Ca 2+的相对量。为了改善对释放的Ca 2+的检测，通过使用含有0.5 mM La 3+的名义上不含Na+/Ca（2+）的培养基来最大限度地减少Ca 2+从细胞质中的挤出[对于血管收缩实验，培养基含有0.5 mM乙二醇-双（β-氨基乙醚）-N，N，N '，N'-四乙酸且不含La 3 +]。Ca 2+释放由SR Ca（2+）-ATP酶抑制剂毒胡萝卜素（TG）以及血管收缩剂精氨酸加压素（AVP）和5-羟色胺（5-HT）触发。用1-3 mM哇巴因孵育20 min，将[Na+]cyt从4.4 mM升高至9.0 mM，仅轻微增加“静息”[Ca 2 +]cyt（从87 nM升高至122 nM）。然而，哇巴因大大增加了由TG（从639 nM（对照）到1，021 nM），AVP（从993到1，597 nM）和5-HT（从559到1，486 nM）引起的Ca 2+释放。哇巴因诱导的TG-诱发的Ca 2+释放的增强不受10 μ M维拉帕米的影响;这意味着哇巴因的作用不是由于通过电压门控Ca 2+通道的Ca 2+进入。当哇巴因在无Na（+）的培养基（Na+被等摩尔的N-甲基-D-葡糖胺替代）中应用20 min以防止[Na+]cyt升高时，对TG的反应没有增强。（250字处删节）
The effect of a rise in intracellular Na+ concentration ([Na+]cyt) on the amount of Ca2+ in intracellular stores was studied in vascular smooth muscle cells from the A7r5 line. The relative amount of stored Ca2+ was estimated in fura 2-loaded cells by the rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) evoked by Ca2+ release from the sarcoplasmic reticulum (SR). To improve the detection of released Ca2+, extrusion of Ca2+ from the cytosol was minimized by using nominally Na+/Ca(2+)-free medium containing 0.5 mM La3+ [for vasoconstrictor experiments, the medium contained 0.5 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid and no La3+]. Ca2+ release was triggered by thapsigargin (TG), an SR Ca(2+)-ATPase inhibitor, and by the vasoconstrictors arginine vasopressin (AVP) and serotonin (5-HT). Incubation with 1-3 mM ouabain for 20 min, which raises [Na+]cyt from 4.4 to 9.0 mM, increased "resting" [Ca2+]cyt only slightly (from 87 to 122 nM). However, ouabain greatly augmented the release of Ca2+ evoked by TG [from 639 nM (control) to 1,021 nM], by AVP (from 993 to 1,597 nM), and by 5-HT (from 559 to 1,486 nM). Ouabain-induced augmentation of TG-evoked Ca2+ release was not affected by 10 microM verapamil; this implies that the effect of ouabain was not due to Ca2+ entry through voltage-gated Ca2+ channels. The response to TG was not augmented when ouabain was applied for 20 min in Na(+)-free medium (Na+ replaced by equimolar N-methyl-D-glucamine) to prevent [Na+]cyt from rising.(ABSTRACT TRUNCATED AT 250 WORDS)