{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T16:38:07Z","timestamp":1789231087567,"version":"build-2803163510"},"reference-count":43,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2011,9,28]],"date-time":"2011-09-28T00:00:00Z","timestamp":1317168000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p>\n                    Increased vascular smooth muscle contractility has an important role in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). Myofilament Ca\n                    <jats:sup>2+<\/jats:sup>\n                    sensitivity is a major determinant of smooth muscle contractility. We investigated changes in the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -sensitizing effect of endothelin-1 (ET-1) and the mechanisms underlying ET-1-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    sensitization after SAH using a rabbit SAH model. After SAH, the contractile response to ET-1 was enhanced, and the ET\n                    <jats:sub>A<\/jats:sub>\n                    receptor expression was upregulated in the basilar artery. In \u03b1-toxin-permeabilized preparations, ET-1 induced enhanced and prolonged contraction after SAH, suggesting that ET-1-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    sensitization is potentiated after SAH. Endothelin-1-induced Ca\n                    <jats:sup>2+<\/jats:sup>\n                    sensitization became less sensitive to inhibitors of Rho-associated coiled-coil protein kinase (ROCK) and protein kinase C (PKC) after SAH. The expression of PKC\u03b1, ROCK2, PKC-potentiated phosphatase inhibitor of 17\u2009kDa (CPI-17) and myosin phosphatase target subunit 1 (MYPT1) was upregulated, and the level of phosphorylation of CPI-17 and MYPT1 was elevated after SAH. This study demonstrated for the first time that the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -sensitizing effect of ET-1 on myofilaments is potentiated after SAH. The increased expression and activity of PKC\u03b1, ROCK2, CPI-17, and MYPT1, as well as the upregulation of ET\n                    <jats:sub>A<\/jats:sub>\n                    receptor expression are suggested to underlie the enhanced and prolonged Ca\n                    <jats:sup>2+<\/jats:sup>\n                    sensitization induced by ET-1.\n                  <\/jats:p>","DOI":"10.1038\/jcbfm.2011.132","type":"journal-article","created":{"date-parts":[[2011,9,28]],"date-time":"2011-09-28T04:21:49Z","timestamp":1317183709000},"page":"341-352","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":23,"title":["Mechanisms Underlying Potentiation of Endothelin-1-Induced Myofilament Ca\n                    <sup>2+<\/sup>\n                    Sensitization after Subarachnoid Hemorrhage"],"prefix":"10.1177","volume":"32","author":[{"given":"Yuichiro","family":"Kikkawa","sequence":"first","affiliation":[{"name":"Division 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