Comparison of the Effects of Endothelin-1, -2 and -3 (1 - 31) on Changes in [Ca2+]i in Human Coronary Artery Smooth Muscle Cells

The Japanese Journal of Pharmacology

Masanori Yoshizumi¹  Hiroshi Kido³  Hiroaki Yasuoka¹  Kazuyoshi Kirima¹  Toshiaki Tamaki¹  Daisuke Inui¹  Hitoshi Houchi²  Mami Azuma²  Koichiro Tsuchiya¹ 

[1] Department of Pharmacology, The University of Tokushima School of Medicine;Department of Pharmacy, The University of Tokushima School of Medicine;Division of Enzyme Chemistry, The Institute for Enzyme Research, The University of Tokushima

关键词: Endothelins (1 - 31);    Endothelins (1 - 21);    Human chymase;    Confocal laser microscopy;    Intracellular free Ca2+;   

DOI  :  10.1254/jjp.81.298

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(27)Cited-By(4)We have previously found that human chymase selectively cleaves big endothelins (ETs) at the Tyr31-Gly32 bond to produce 31-amino-acid endothelins, ETs (1 - 31). In the present study, we investigated the effects of ETs (1 - 31) on changes in intracellular free Ca2+ ([Ca2+]i) in cultured human coronary artery smooth muscle cells (HCASMCs) using confocal laser microscopy. ETs (1 - 31) increased [Ca2+]i in a concentration-dependent manner. Phosphoramidon did not inhibit the increases in [Ca2+]i caused by ETs (1 - 31). The [Ca2+]i increases induced by ETs (1 - 31) were compared to those of ETs (1 - 21) and big ETs. ET-1 (1 - 21) was about 10-times more potent than big ET-1 or ET-1 (1 - 31), whereas big ET-2 was 10-times less potent than ET-2 (1 - 21) or ET-2 (1 - 31). ETs (1 - 31) may induce [Ca2+]i increase through ETA-type or ETA-type-like receptors. The 10-12 M ET (1 - 31)-induced increases in [Ca2+]i were not affected by removal of extracellular Ca2+, but were inhibited by thapsigargin. These results suggested that ET-1, -2 and -3 (1 - 31) showed similar potencies in increasing [Ca2+]i and mechanisms of ET (1 - 31)-induced increases in [Ca2+]i may be similar among the three ETs (1 - 31).

【 授权许可】

Unknown