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首页> 外文期刊>Japanese Journal of Pharmacology >Different Pathways for Ca2+ Influx and Intracellular Release of Ca2+ Mediated by Muscarinic Receptors in Ileal Longitudinal Smooth Muscle
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Different Pathways for Ca2+ Influx and Intracellular Release of Ca2+ Mediated by Muscarinic Receptors in Ileal Longitudinal Smooth Muscle

机译：回肠纵向平滑肌中毒蕈碱受体介导的Ca2 +内流和Ca2 +释放的不同途径

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References(33) Cited-By(12) Muscarinic receptor-mediated elevations in intracellular Ca2+ concentration ([Ca2+]i) in the longitudinal smooth muscle of guinea pig ileum were studied by the use of fura-2 fluorescence. Dose-response analysis indicated a difference in the potencies of carbachol (CCh) to increase [Ca2+]i in the presence and absence of extracellular Ca2+. For the increase in [Ca2+]i due to Ca2+ release from intracellular stores in the absence of extracellular Ca2+, the ED50 value of CCh was 3 × 10-5 M. On the other hand, in the presence of Ca2+, the ED50 value was 2.5 × 10-7 M, indicating that a low concentration of CCh ( 10-7 M) caused influx of extracellular Ca2+ without Ca2+ release. Oxotremorine and pilocarpine induced Ca2+ influx, but were less potent inducers of Ca2+ release. CCh also stimulated the formation of inositol trisphosphates (IP3) with an ED50 value of (4.5 × 10-5 M), which was similar to that for Ca2+ release from intracellular stores. Treatment of the smooth muscle with neomycin (1 mM), a phospholipase C inhibitor, abolished both CCh-induced IP3 formation and Ca2+ release from intracellular stores, but did not affect CCh-induced Ca2+ influx. These results suggest that the pathway for muscarinic stimulation of Ca2+ influx through plasma membranes is different from that for Ca2+ release from intracellular stores, which seems to be coupled with IP3 formation.
机译：参考文献（33）用Fura-2荧光技术研究了豚鼠回肠纵向平滑肌中毒蕈碱受体介导的胞内Ca2 +浓度（[Ca2 +] i）升高。剂量反应分析表明，存在和不存在细胞外Ca2 +时，卡巴胆碱（CCh）增加[Ca2 +] i的效力不同。对于在不存在细胞外Ca2 +的情况下由于Ca2 +从细胞内存储释放而导致的[Ca2 +] i的增加，CCh的ED50值为3×10-5M。另一方面，在存在Ca2 +的情况下，ED50值为2.5×10-7 M，表明低浓度的CCh（<10-7 M）导致细胞外Ca2 +流入而没有Ca2 +释放。 Oxotremorine和毛果芸香碱诱导Ca2 +大量涌入，但对Ca2 +释放的诱导作用较弱。 CCh还刺激ED50值为（4.5×10-5 M）的肌醇三磷酸酯（IP3）的形成，这与细胞内存储中Ca2 +的释放相似。用磷脂酶C抑制剂新霉素（1 mM）处理平滑肌，可消除CCh诱导的IP3形成和细胞内存储中Ca2 +的释放，但不影响CCh诱导的Ca2 +流入。这些结果表明，毒蕈碱刺激质膜上的Ca2 +流入的途径不同于细胞内存储中Ca2 +释放的途径，这似乎与IP3的形成有关。

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