Potentiation by endothelin-1 of Ca2+ sensitivity of contractile elements depends on Ca2+ influx through L-type Ca2+ channels in the canine cerebral artery |
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| Affiliation: | 1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China;2. National Resource Center for Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China;3. College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China;4. Biology Department, Cornell University, Ithaca, NY 14850, United States of America;5. Shaanxi Academy of Traditional Chinese Medicine, Xi''an 710003, China;6. China Academy of Chinese Medical Sciences, Beijing 100700, China;7. Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3800, Australia;8. School of Pharmaceutical Science, Shandong University, Shandong 250100, China;9. Qilu Hospital, Cheeloo College of Medicine, Shandong University, Shandong 250100, China;1. Department of Materials Science and Engineering, Indian Institute of Technology Kanpur, Kanpur 208016, India;2. Department of Mechanical Engineering, Indian Institute of Science Bangalore, 560012, Karnataka, India;3. Advanced Centre for Materials Science, Indian Institute of Technology Kanpur, Kanpur 208016, India |
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| Abstract: | - 1.1. Endothelin-1 (ET-1) contracted canine cerebral artery in a concentration-dependent manner with an increase in intracellular Ca2+ concentration ([Ca2+]i), and at higher concentrations it produced a greater contraction with a smaller increase in [Ca2+]i.
- 2.2. Ca2+ channel antagonist such as d-cis-diltiazem inhibited the tension more effectively than the [Ca2+]i increased by ET-1.
- 3.3. In Ca2+-free solution containing 0.2 mM EGTA, ET-1 elicited a transient increase in [Ca2+]i and tension.
- 4.4. In the Staphylococcus aureus α-toxin-permeabilized artery, ET-1 shifted the pCa-tension relationship leftwards in the presence of GTP.
- 5.5. These findings suggest that ET-I contracts the canine cerebral artery by increasing not only the Ca2+ influx through L-type Ca2+ channels, but also Ca2+ release from the intracellular storage sites, and also Ca2+ sensitivity of contractile elements. The degree of Ca2+ sensitivity is strongly affected by [Ca2+]i which is increased by the Ca2+ influx through L-type Ca2+ channels.
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