{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,26]],"date-time":"2025-09-26T22:34:24Z","timestamp":1758926064883},"reference-count":37,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2013,2,6]],"date-time":"2013-02-06T00:00:00Z","timestamp":1360108800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Prostate"],"published-print":{"date-parts":[[2013,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>Prostate smooth muscle plays an important role in the physiological ejection of prostatic fluid and also in the pathogenesis of benign prostate hyperplasia. Although mouse is the best genetically engineered animal model to identify potential molecular targets for human diseases, only fragmentary information is available for basic mechanism of mouse prostate contraction.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>Small smooth muscle tubular rings were excised from four mouse prostate lobes to measure their isometric contractions. High K<jats:sup>+<\/jats:sup>, noradrenaline (NA), or acetylcholine (ACh) was applied with and without various antagonists and\/or inhibitors to examine the contractile signaling pathways.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>Maximum amplitude of agonist\u2010induced contractions varied greatly with different lobes but not with different locations or orientations within each lobe. Both NA and ACh produced large contractions in ventral and dorsal rings, whereas only small contractions were elicited in lateral and anterior rings. Combination of alpha\u20101 and muscarinic antagonists suppressed K<jats:sup>+<\/jats:sup> depolarization\u2010induced contraction potently in ventral rings, but slightly in anterior rings. Blocking of either Ca<jats:sup>2+<\/jats:sup>\u2010release or Ca<jats:sup>2+<\/jats:sup>\u2010influx reduced agonist\u2010induced contraction of ventral rings, however, a considerable amount of contractility remained even with both blockers. Inhibitors of ROCK and PKC partially inhibited NA\u2010induced contractions, whereas a combination of Ca<jats:sup>2+<\/jats:sup>\u2010blockers and Ca<jats:sup>2+<\/jats:sup>\u2010sensitization inhibitors strongly suppressed the contraction.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS<\/jats:title><jats:p>The ejection of prostatic fluid is differentially regulated in each prostate lobe. In ventral prostate smooth muscle, Ca<jats:sup>2+<\/jats:sup>\u2010release, Ca<jats:sup>2+<\/jats:sup>\u2010influx, and ROCK\u2010 and PKC\u2010mediated Ca<jats:sup>2+<\/jats:sup>\u2010sensitizations are all involved in NA\u2010induced contractions. This finding is a useful step toward the understanding of the phenotypic changes in the smooth muscle of BPH prostate. Prostate 73: 996\u20131006, 2013. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/pros.22647","type":"journal-article","created":{"date-parts":[[2013,2,6]],"date-time":"2013-02-06T13:12:57Z","timestamp":1360156377000},"page":"996-1006","source":"Crossref","is-referenced-by-count":5,"title":["Contractile signaling pathways in mouse prostate smooth 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