{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T19:14:49Z","timestamp":1757704489921},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,2,4]],"date-time":"2005-02-04T00:00:00Z","timestamp":1107475200000},"content-version":"vor","delay-in-days":3567,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Reproduction Devel"],"published-print":{"date-parts":[[1995,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>This study investigated the underlying mechanisms of oxytocin (OT)\u2010induced increases in intracellular Ca<jats:sup>2+<\/jats:sup> concentrations ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) in acutely dispersed myometrial cells from prepartum sows. A dosedependent increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> was induced by OT (0.1 nM to 1 \u03bcM) in the presence and absence of extracellular Ca<jats:sup>2+<\/jats:sup> ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>e<\/jats:sub>). [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> was elevated by OT in a biphasic pattern, with a spike followed by a sustained plateau in the presence of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>e<\/jats:sub>. However, in the absence of [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>e<\/jats:sub>, the [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> response to OT became monophasic with a lower amplitude and no plateau, and this monophasic increase was abolished by pretreatment with ionomycin, a Ca<jats:sup>2+<\/jats:sup> ionophore. Administration of OT (1 \u03bcM) for 15 sec increased inositol 1,4,5\u2010trisphosphate (IP<jats:sub>3<\/jats:sub>) formation by 61%. Pretreatment with pertussis toxin (PTX, 1 \u03bcg\/ml) for 2 hr failed to alter the OT\u2010induced increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and IP<jats:sub>3<\/jats:sub> formation. U\u201073122 (30 nM to 3 \u03bcM), a phospholipase C (PLC) inhibitor, depressed the rise in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> by OT dose dependently. U\u201073122 (3 \u03bcM) also abolished the OT\u2010induced IP<jats:sub>3<\/jats:sub> formation. Thapsigargin (2 \u03bcM), an inhibitor of Ca<jats:sup>2+<\/jats:sup>\u2010ATPase in the endoplasmic reticulum, did not increase [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. However, it did time\u2010dependently inhibit the OT\u2010induced increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Nimodipine (1 \u03bcM), a Voltage\u2010dependent Ca<jats:sup>2+<\/jats:sup> channel (VDCC) blocker, inhibited the OT\u2010induced plateau by 26%. La<jats:sup>3+<\/jats:sup> (1 \u03bcM), a nonspecific Ca<jats:sup>2+<\/jats:sup> channel blocker, abrogated the OT\u2010induced plateau. In whole\u2010cell patch\u2010clamp studies used to evaluate VDCC activities, OT (0.1 \u03bcM) increased Ca<jats:sup>2+<\/jats:sup> Current (I<jats:sub>ca<\/jats:sub>) by 40% with no apparent changes in the current\u2010voltage relationship. The OT\u2010induced increase in I<jats:sub>ca<\/jats:sub> reached the maximum in 5 min, and the increase was abolished by nimodipine (1 \u03bcM). These results suggested that (1) activation of OT receptors in porcine myometrium evokes a cascade in the PTX\u2010insensitive G\u2010protein\u2013PLC\u2010IP<jats:sub>3<\/jats:sub> signal transduction, resulting in an increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>; (2) the OT\u2010induced increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> is characterized by a biphasic pattern, in which the spike is predominately contributed by the intracellular Ca<jats:sup>2+<\/jats:sup> release from the IP<jats:sub>3<\/jats:sub>\u2010sensitive pool, and to a lesser extent by Ca<jats:sup>2+<\/jats:sup> influx, whereas the plateau is from increased Ca<jats:sup>2+<\/jats:sup> influx; and (3) the influx is via VDCC and receptor\u2010operated Ca<jats:sup>2+<\/jats:sup> channels. \u00a9 1995 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mrd.1080410105","type":"journal-article","created":{"date-parts":[[2005,2,23]],"date-time":"2005-02-23T23:07:06Z","timestamp":1109200026000},"page":"20-28","source":"Crossref","is-referenced-by-count":14,"title":["Oxytocin induced a biphasic increase in the intracellular Ca<sup>2+<\/sup> concentration of porcine myometrial cells: Participation of a pertussis toxin\u2014insensitive G\u2010protein, inositol 1,4,5\u2010trisphosphate\u2014sensitive Ca<sup>2+<\/sup> pool, and Ca<sup>2+<\/sup> channels"],"prefix":"10.1002","volume":"41","author":[{"given":"Ronghua","family":"Zhuge","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Siben","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ter\u2010Hsin","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Walter H.","family":"Hsu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,2,4]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1210\/endo-124-1-17"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(86)90639-4"},{"key":"e_1_2_1_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/361315a0"},{"key":"e_1_2_1_5_1","doi-asserted-by":"crossref","first-page":"21486","DOI":"10.1016\/S0021-9258(20)80564-X","article-title":"Inhibition of thapsigargin\u2010induced calcium entry by microinjected guanine nucleotide analogues. 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