MAGNESIUM RELAXES ARTERIAL SMOOTH-MUSCLE BY DECREASING INTRACELLULAR CA2+ WITHOUT CHANGING INTRACELLULAR MG2+
MAGNESIUM RELAXES ARTERIAL SMOOTH-MUSCLE BY DECREASING INTRACELLULAR CA2+ WITHOUT CHANGING INTRACELLULAR MG2+
复制标题
DOI：
10.1172/jci115807
复制
发表时间：
1992-06-01
影响因子：
15.9
通讯作者：
REMBOLD, CM
中科院分区：
文献类型：
--
作者：
DANGELO, EKG;SINGER, HA;REMBOLD, CM
细胞外[Mg 2 +]（[Mg 2 +]o）的升高使血管平滑肌松弛。我们测试了升高的[Mg 2 +]o通过减少肌浆[Ca 2 +]和肌球蛋白轻链磷酸化而不改变细胞内[Mg 2 +]（[Mg 2 +]i）诱导松弛的假设。组胺刺激无内皮的猪颈动脉中膜组织与Fura 2和水母发光蛋白估计的肌浆[Ca 2 +]、肌球蛋白磷酸化和力的增加相关。升高的[Mg 2 +]o降低肌浆[Ca 2 +]和力至接近静息值。然而，升高的[Mg 2 +]o仅短暂降低肌球蛋白磷酸化值：持续的[Mg 2 +] o诱导的肌浆[Ca 2 +]和力的降低与不适当的高肌球蛋白磷酸化值相关。在[Mg 2 +] o诱导的松弛过程中，肌球蛋白磷酸化水平升高完全是在丝氨酸19上，丝氨酸19是Ca 2 +/钙调蛋白依赖性肌球蛋白轻链激酶底物。肌浆[Mg 2 +]（用Mag-Fura 2估计）不随[Mg 2 +]o升高而显著增加。这些结果与[Mg ~（2+）]_o增加通过降低肌浆[Ca ~（2+）]而不改变[Mg ~（2+）]_i诱导松弛的假设一致。这些数据还表明肌球蛋白磷酸化从肌浆[Ca 2 +]和力在Mg 2+诱导的松弛过程中的解离。这一发现表明，存在一个磷酸化独立的（但潜在的Ca 2+依赖）的机制，调节血管平滑肌的力量。
Elevations in extracellular [Mg2+] ([Mg2+]o) relax vascular smooth muscle. We tested the hypothesis that elevated [Mg2+]o induces relaxation through reductions in myoplasmic [Ca2+] and myosin light chain phosphorylation without changing intracellular [Mg2+] ([Mg2+]i). Histamine stimulation of endothelium-free swine carotid medial tissues was associated with increases in both Fura 2- and aequorin-estimated myoplasmic [Ca2+], myosin phosphorylation, and force. Elevated [Mg2+]o decreased myoplasmic [Ca2+] and force to near resting values. However, elevated [Mg2+]o only transiently decreased myosin phosphorylation values: sustained [Mg2+]o-induced decreases in myoplasmic [Ca2+] and force were associated with inappropriately high myosin phosphorylation values. The elevated myosin phosphorylation during [Mg2+]o-induced relaxation was entirely on serine 19, the Ca2+/calmodulin-dependent myosin light chain kinase substrate. Myoplasmic [Mg2+] (estimated with Mag-Fura 2) did not significantly increase with elevated [Mg2+]o. These results are consistent with the hypothesis that increased [Mg2+]o induces relaxation by decreasing myoplasmic [Ca2+] without changing [Mg2+]i. These data also demonstrate dissociation of myosin phosphorylation from myoplasmic [Ca2+] and force during Mg2+-induced relaxation. This finding suggests the presence of a phosphorylation-independent (yet potentially Ca2+-dependent) mechanism for regulation of force in vascular smooth muscle.