Todoroki-Ikeda N, Mizukami Y, Mogami K, Kusuda T, Yamamoto K, Miyake T, Sato M, Suzuki S, Yamagata H, Hokazono Y, Kobayashi S
First Department of Physiology, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube 755-8505, Japan.
FEBS Lett. 2000 Sep 29;482(1-2):85-90. doi: 10.1016/s0014-5793(00)02046-9.
Sphingosylphosphorylcholine (SPC), a sphingolipid, concentration-dependently (1-50 microM) induced contraction and slight elevation of the cytosolic Ca(2+) concentration (Ca(2+)) in smooth muscle of the pig coronary artery, the result being a marked increase in the force/Ca(2+) ratio. In alpha-toxin- or beta-escin-permeabilized, but not Triton X-100-permeabilized, vascular strips, SPC induced contraction at constant Ca(2+) (pCa 6.3) in the absence of GTP, whereas a G-protein-coupled receptor agonist, histamine, required the presence of GTP to induce the contraction. The Rho-kinase blocker, Y-27632 (10 microM) abolished the SPC-induced Ca(2+)-sensitization, without affecting the Ca(2+)-induced contraction. These results suggest that SPC induces Ca(2+)-sensitization of force in vascular smooth muscle, presumably through the activation of Rho-kinase (or a related kinase).
鞘氨醇磷酸胆碱(SPC),一种鞘脂,以浓度依赖方式(1 - 50微摩尔)诱导猪冠状动脉平滑肌收缩,并使胞质Ca(2+)浓度(Ca(2+))略有升高,结果是力/Ca(2+)比值显著增加。在经α-毒素或β-七叶皂苷通透但未经 Triton X - 100通透的血管条中,SPC在无GTP的情况下于恒定Ca(2+)(pCa 6.3)时诱导收缩,而G蛋白偶联受体激动剂组胺则需要GTP存在才能诱导收缩。Rho激酶阻断剂Y - 27632(10微摩尔)消除了SPC诱导的Ca(2+)敏感性增强,而不影响Ca(2+)诱导的收缩。这些结果表明,SPC可能通过激活Rho激酶(或相关激酶)诱导血管平滑肌中力的Ca(2+)敏感性增强。