Magnesium as a modifier of smooth muscle contractility.

H Karaki
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Abstract

In smooth muscle, Ca2+ enters the cell through two different types of Ca2+ channels, activates contractile filaments and induces contraction. These Ca2+ channels are inhibited by Ca2+ channel blockers and/or nitrocompounds. Mg2+ inhibits both of these Ca2+ channels and relaxes the muscle. A portion of the smooth muscle contraction is due also to the release of Ca2+ from the cellular storage site. Caffeine and norepinephrine release Ca2+ from this store to induce a transient contraction. The contraction induced by caffeine is greatly augmented in the absence of Mg2+. The other effect of Mg2+ deficiency is to inhibit the effects of various vasodilators. Vascular endothelium releases a substance which relaxes vascular smooth muscle and this relaxation is also inhibited by Mg2+ deficiency. Thus, Mg2+ has multiple sites and mechanisms of action in smooth muscle which remain to be clarified.

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镁作为平滑肌收缩性的调节剂。
在平滑肌中,Ca2+通过两种不同类型的Ca2+通道进入细胞,激活收缩细丝并诱导收缩。这些Ca2+通道被Ca2+通道阻滞剂和/或硝基化合物抑制。Mg2+抑制这两种Ca2+通道并放松肌肉。平滑肌收缩的一部分也是由于Ca2+从细胞储存部位释放。咖啡因和去甲肾上腺素释放Ca2+,引起短暂的收缩。在没有Mg2+的情况下,咖啡因引起的收缩大大增强。Mg2+缺乏的另一个作用是抑制各种血管扩张剂的作用。血管内皮释放一种使血管平滑肌松弛的物质,这种松弛也因Mg2+缺乏而受到抑制。因此,Mg2+在平滑肌中有多个位点和作用机制尚待阐明。
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