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首页> 外文期刊>American Journal of Physiology >Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.
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Effects of estradiol on phenylephrine contractility associated with intracellular calcium release in rat aorta.

机译：雌二醇对与大鼠主动脉细胞内钙释放有关的去氧肾上腺素收缩力的影响。

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摘要

The ability of estradiol to affect phenylephrine-induced contraction and the subsequent increase in resting tone, associated with capacitative Ca(2+) entry across the plasma membrane, was evaluated in rat aortic rings incubated in Ca(2+)-free solution. The incubation with estradiol (1-100 nM, 5 min) inhibited both the phenylephrine-induced contraction and the IRT. Neither cycloheximide (1 microM; inhibitor of protein synthesis) nor tamoxifen (1 microM; blocker of estrogenic receptors) modified the effects of estradiol. Estradiol (100 microM) also blocked the contractile response to serotonin (10 microM) but not to caffeine (10 mM). In addition, estradiol (100 microM) inhibited the contractile responses to cyclopiazonic acid (1 microM; selective Ca(2+)-ATPase inhibitor) associated with capacitative Ca(2+) influx through non-L-type Ca(2+) channels. Finally, estradiol inhibited the Ca(2+)-induced increases in intracellular free Ca(2+) (after pretreatment with phenylephrine) in cultured rat aorta smooth muscle cells incubated in Ca(2+)-free solution. In conclusion, estradiol interfered in a concentration-dependent manner with Ca(2+)-dependent contractile effects mediated by the stimuli of alpha(1)-adrenergic and serotonergic receptors and inhibited the capacitative Ca(2+) influx through both L-type and non-L-type Ca(2+) channels. Such effects are in essence nongenomic and not mediated by the intracellular estrogenic receptor.
机译：雌二醇影响去氧肾上腺素诱导的收缩和随后的休息音的增加，与电容性Ca（2+）穿过质膜进入相关的能力，在无Ca（2+）溶液中培养的大鼠主动脉环中进行了评估。用雌二醇孵育（1-100 nM，5分钟）可抑制去氧肾上腺素引起的收缩和IRT。环己酰亚胺（1 microM;蛋白质合成抑制剂）和他莫昔芬（1 microM;雌激素受体阻滞剂）均未改变雌二醇的作用。雌二醇（100 microM）也阻断了对血清素（10 microM）的收缩反应，但没有阻断对咖啡因（10 mM）的收缩反应。此外，雌二醇（100 microM）抑制对环吡嗪酸（1 microM;选择性Ca（2 +）-ATPase抑制剂）的收缩反应，与通过非L型Ca（2+）通道的Ca（2+）流入相关。最后，雌二醇抑制培养的大鼠主动脉平滑肌细胞中无Ca（2+）溶液中培养的Ca（2+）诱导的细胞内游离Ca（2+）的增加（用去氧肾上腺素预处理后）。总之，雌二醇以浓度依赖性方式干扰由α（1）-肾上腺素能和5-羟色胺能受体的刺激介导的Ca（2+）依赖性收缩作用，并通过两种L型抑制电容性Ca（2+）流入。和非L型Ca（2+）通道。这种作用本质上是非基因组的，并且不是由细胞内雌激素受体介导的。

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