{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:18:06Z","timestamp":1718651886341},"reference-count":35,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2005,3]]},"abstract":"<jats:p> A hyposmotic challenge elicited contraction of isolated canine basilar arteries. The contractile response was nearly abolished by the removal of extracellular Ca<jats:sup>2+<\/jats:sup> and by the voltage-dependent Ca<jats:sup>2+<\/jats:sup> channel (VDCC) blocker nicardipine, but it was unaffected by thapsigargin, which depletes intracellular Ca<jats:sup>2+<\/jats:sup> stores. The contraction was also inhibited by Gd<jats:sup>3+<\/jats:sup> and ruthenium red, cation channel blockers, and Cl<jats:sup>\u2212<\/jats:sup> channel blockers DIDS and niflumic acid. The reduction of extracellular Cl<jats:sup>\u2212<\/jats:sup> concentrations enhanced the hypotonically induced contraction. Patch-clamp analysis showed that a hyposmotic challenge activated outwardly rectifying whole cell currents in isolated canine basilar artery myocytes. The reversal potential of the current was shifted toward negative potentials by reductions in intracellular Cl<jats:sup>\u2212<\/jats:sup> concentration, indicating that the currents were carried by Cl<jats:sup>\u2212<\/jats:sup>. Moreover, the currents were abolished by 10 mM BAPTA in the pipette solution and by the removal of extracellular Ca<jats:sup>2+<\/jats:sup>. Taken together, these results suggest that a hyposmotic challenge activates cation channels, which presumably cause Ca<jats:sup>2+<\/jats:sup> influx, thereby activating Ca<jats:sup>2+<\/jats:sup>-activated Cl<jats:sup>\u2212<\/jats:sup> channels. The subsequent membrane depolarization is likely to increase Ca<jats:sup>2+<\/jats:sup> influx through VDCC and elicit contraction. <\/jats:p>","DOI":"10.1152\/ajpcell.00367.2003","type":"journal-article","created":{"date-parts":[[2004,11,4]],"date-time":"2004-11-04T01:13:54Z","timestamp":1099530834000},"page":"C702-C709","source":"Crossref","is-referenced-by-count":11,"title":["Ionic mechanism for contractile response to hyposmotic challenge in canine basilar arteries"],"prefix":"10.1152","volume":"288","author":[{"given":"Shunsuke","family":"Yano","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomohisa","family":"Ishikawa","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hidetaka","family":"Tsuda","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuo","family":"Obara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Koichi","family":"Nakayama","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"R1","doi-asserted-by":"crossref","unstructured":"Ackerman MJ, Wickman KD, and Clapham DE. 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