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血管收缩激素在培养的大鼠血管平滑肌细胞中的细胞作用机制。

The cellular mechanism of action by vasoconstrictor hormones in cultured rat vascular smooth muscle cells.

作者信息

Takata S, Hirata Y, Takagi Y, Fukase M, Fujita T

机构信息

Department of Medicine, Kobe University School of Medicine, Japan.

出版信息

Am J Hypertens. 1990 Aug;3(8 Pt 2):227S-230S. doi: 10.1093/ajh/3.8.227.

Abstract

The effects of angiotensin (Ang) II, arginine vasopressin (AVP), and serotonin (5-HT) on inositol trisphosphate (IP3) production, cytosolic Ca2+ concentration [( Ca2+]i), and the phosphorylation of 20 kilodalton myosin light chain (MLC) were examined in cultured rat vascular smooth muscle cells (VSMC). These vasoconstrictors immediately induced dose-dependent and concomitant increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC. The agonist-induced increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC in VSMC were completely blocked by pretreatment with the receptor antagonists for Ang II, V1, and 5-HT2, respectively. These data suggest that receptor-mediated increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC by these vasoconstrictors are closely interrelated.

摘要

在培养的大鼠血管平滑肌细胞(VSMC)中,研究了血管紧张素(Ang)II、精氨酸加压素(AVP)和血清素(5-HT)对三磷酸肌醇(IP3)生成、胞质钙离子浓度[Ca2+]i以及20千道尔顿肌球蛋白轻链(MLC)磷酸化的影响。这些血管收缩剂可立即诱导IP3生成、[Ca2+]i以及20 kDa MLC磷酸化呈剂量依赖性且同时增加。血管紧张素II、V1和5-HT2的受体拮抗剂预处理分别完全阻断了激动剂诱导的VSMC中IP3生成、[Ca2+]i以及20 kDa MLC磷酸化的增加。这些数据表明,这些血管收缩剂通过受体介导的IP3生成、[Ca2+]i以及20 kDa MLC磷酸化的增加密切相关。

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