{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T18:58:19Z","timestamp":1791917899912,"version":"4.3.4"},"reference-count":45,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":425,"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":[[2007,12]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>Electrically active atypical smooth muscle cells (ASMCs) within the renal pelvis have long been considered to act as pacemaker cells driving pelviureteric peristalsis. We have investigated the role of Ca<jats:sup>2+<\/jats:sup>entry and uptake into and release from internal stores in the generation of Ca<jats:sup>2+<\/jats:sup>transients and spontaneous transient depolarizations (STDs) in ASMCs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>The electrical activity and separately visualized changes in intracellular Ca<jats:sup>2+<\/jats:sup>concentration in typical smooth muscle cells (TSMCs), ASMCs and interstitial cells of Cajal\u2010like cells (ICC\u2010LCs) were recorded using intracellular microelectrodes and a fluorescent Ca<jats:sup>2+<\/jats:sup>indicator, fluo\u20104.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>In 1 \u03bc<jats:sc>M<\/jats:sc>nifedipine, high frequency (10\u201330\u2003min<jats:sup>\u22121<\/jats:sup>) Ca<jats:sup>2+<\/jats:sup>transients and STDs were recorded in ASMCs, while ICC\u2010LCs displayed low frequency (1\u20133\u2003min<jats:sup>\u22121<\/jats:sup>) Ca<jats:sup>2+<\/jats:sup>transients. All spontaneous electrical activity and Ca<jats:sup>2+<\/jats:sup>transients were blocked upon removal of Ca<jats:sup>2+<\/jats:sup>from the bathing solution, blockade of Ca<jats:sup>2+<\/jats:sup>store uptake with cyclopiazonic acid (CPA) and with 2\u2010aminoethoxy\u2010diphenylborate (2\u2010APB). STD amplitudes were reduced upon removal of the extracellular Na<jats:sup>+<\/jats:sup>or blockade of IP<jats:sub>3<\/jats:sub>dependent Ca<jats:sup>2+<\/jats:sup>store release with neomycin or U73122. Blockade of ryanodine\u2010sensitive Ca<jats:sup>2+<\/jats:sup>release blocked ICC\u2010LC Ca<jats:sup>2+<\/jats:sup>transients but only reduced Ca<jats:sup>2+<\/jats:sup>transient discharge in ASMCs. STDs in ASMCS were also little affected by DIDS, La<jats:sup>3+<\/jats:sup>, Gd<jats:sup>3+<\/jats:sup>or by the replacement of extracellular Cl<jats:sup>\u2010<\/jats:sup>with isethionate.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>ASMCs generated Ca<jats:sup>2+<\/jats:sup>transients and cation\u2010selective STDs via mechanisms involving Ca<jats:sup>2+<\/jats:sup>release from IP<jats:sub>3<\/jats:sub>\u2010dependent Ca<jats:sup>2+<\/jats:sup>stores, STD stimulation of TSMCs was supported by Ca<jats:sup>2+<\/jats:sup>entry through L type Ca<jats:sup>2+<\/jats:sup>channels and Ca<jats:sup>2+<\/jats:sup>release from ryanodine\u2010sensitive stores.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic>(2007)<jats:bold>152<\/jats:bold>, 1248\u20131259; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0707535\">10.1038\/sj.bjp.0707535<\/jats:ext-link>; published 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