{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:45:21Z","timestamp":1773308721115,"version":"3.50.1"},"reference-count":24,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNS"],"published-print":{"date-parts":[[2006,8]]},"abstract":"<jats:sec>\n<jats:title>Object<\/jats:title>\n<jats:p>Endothelin 1 (ET-1) is a major cause of cerebral vasospasm after subarachnoid hemorrhage (SAH), and extracellular Ca<jats:sup>++<\/jats:sup> influx plays an essential role in ET-1\u2013induced vasospasm. The authors recently demonstrated that ET-1 activates two types of Ca<jats:sup>++<\/jats:sup>-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and a store-operated Ca<jats:sup>++<\/jats:sup> channel (SOCC) in vascular smooth-muscle cells located in the basilar arteries (BAs) of rabbits. In the present study, they investigate the effects of phospholipase C (PLC) on ET-1\u2013induced activation of these Ca<jats:sup>++<\/jats:sup> channels and BA contraction by using the PLC inhibitor U73122.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Methods<\/jats:title>\n<jats:p>To determine which Ca<jats:sup>++<\/jats:sup> channels are activated via a PLC-dependent pathway, these investigators monitored the intracellular free Ca<jats:sup>++<\/jats:sup> concentration ([Ca<jats:sup>++<\/jats:sup>]<jats:sub>i<\/jats:sub>). The role of PLC in ET-1\u2013induced vascular contraction was examined by performing a tension study of rabbit BA rings.<\/jats:p>\n<jats:p>The U73122 inhibited the ET-1\u2013induced transient increase in [Ca<jats:sup>++<\/jats:sup>]<jats:sub>i<\/jats:sub>, which resulted from mobilization of Ca<jats:sup>++<\/jats:sup>; from the intracellular store. Phospholipase C also inhibited ET-1\u2013induced extracellular Ca<jats:sup>++<\/jats:sup> influx through the SOCC and NSCC-2, but not through the NSCC-1. The U73122 inhibited the ET-1\u2013induced contraction of the rabbit BA rings, which depended on extracellular Ca<jats:sup>++<\/jats:sup> influx through the SOCC and NSCC-2.<\/jats:p><\/jats:sec>\n<jats:sec>\n<jats:title>Conclusions<\/jats:title>\n<jats:p>These results indicate the following. 1) The SOCC and NSCC-2 are stimulated by ET-1 via a PLC-dependent cascade whereas NSCC-1 is stimulated via a PLC-independent cascade. 2) The PLC is involved in the ET-1\u2013induced contraction of rabbit BA rings, which depends on extracellular Ca<jats:sup>++<\/jats:sup> influx through the SOCC and NSCC-2.<\/jats:p><\/jats:sec>","DOI":"10.3171\/jns.2006.105.2.288","type":"journal-article","created":{"date-parts":[[2008,1,24]],"date-time":"2008-01-24T12:37:17Z","timestamp":1201178237000},"page":"288-293","source":"Crossref","is-referenced-by-count":16,"title":["Involvement of phospholipase C in endothelin 1\u2013induced stimulation of Ca++ channels and basilar artery contraction in 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