{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T06:55:58Z","timestamp":1782284158723,"version":"3.54.5"},"reference-count":38,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":3681,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[1999,1]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Using a microelectrode technique, acetylcholine (ACh)\u2010induced membrane potential changes were characterized using various types of inhibitors of K<jats:sup>+<\/jats:sup> and Cl<jats:sup>\u2212<\/jats:sup> channels in rabbit aortic valve endothelial cells (RAVEC).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>High K<jats:sup>+<\/jats:sup> blocked and low K<jats:sup>+<\/jats:sup> potentiated the two ACh\u2010induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh\u2010induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In Ca<jats:sup>2+<\/jats:sup>\u2010free solution or in the presence of Co<jats:sup>2+<\/jats:sup> or Ni<jats:sup>2+<\/jats:sup>, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA\u2010AM\u2010treated cells, ACh produced only a depolarization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>A low concentration of A23187 attenuated the ACh\u2010induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co<jats:sup>2+<\/jats:sup>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>It is concluded that in RAVEC, ACh produces a two\u2010component hyperpolarization followed by a depolarization. It is suggested that ACh\u2010induced Ca<jats:sup>2+<\/jats:sup> release from the storage sites causes a transient hyperpolarization due to activation of ChTX\u2010sensitive K<jats:sup>+<\/jats:sup> channels and that ACh\u2010activated Ca<jats:sup>2+<\/jats:sup> influx causes a sustained hyperpolarization by activating both ChTX\u2010 and apamin\u2010sensitive K<jats:sup>+<\/jats:sup> channels. Both volume\u2010sensitive Cl<jats:sup>\u2212<\/jats:sup> channels and the Na<jats:sup>+<\/jats:sup>\u2010K<jats:sup>+<\/jats:sup>\u2010Cl<jats:sup>\u2212<\/jats:sup> cotransporter probably contribute to the ACh\u2010induced depolarization.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (1999) <jats:bold>126<\/jats:bold>, 19\u201326; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0702262\">10.1038\/sj.bjp.0702262<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0702262","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T19:54:15Z","timestamp":1106942055000},"page":"19-26","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Acetylcholine\u2010induced membrane potential changes in endothelial cells of rabbit aortic valve"],"prefix":"10.1111","volume":"126","author":[{"given":"Masuo","family":"Ohashi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kohichi","family":"Satoh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeo","family":"Itoh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_7_2_1","first-page":"H1465","article-title":"Bidirectional electrical communication between smooth muscle and endothelial cells in the pig coronary artery","volume":"266","author":"B\u00c9NY J.\u2010L.","year":"1994","journal-title":"Am. 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