{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T15:07:33Z","timestamp":1761059253027},"reference-count":27,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2011,12,19]],"date-time":"2011-12-19T00:00:00Z","timestamp":1324252800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:p>It has been suggested that mechanosensitive ion channels initiate myogenic responses in vessels; however, the molecular identity of the mechanosensitive ion channel complex is unknown. Although previous reports have suggested that epithelial Na<jats:sup>+<\/jats:sup> channel (ENaC) proteins are mechanotransducers in arteries, experimental evidence demonstrating that ENaC proteins are mechanotransducers are not fully elucidated. The goal of the present study was to determine whether the ENaC is a mechanotransducer for the myogenic response by providing supporting evidence in the rat posterior cerebral artery (PCA). We measured the effect of ENaC inhibition on the pressure\u2010induced myogenic response, Ca<jats:sup>2+<\/jats:sup> concentration and 20 kDa myosin light chain (MLC<jats:sub>20<\/jats:sub>) phosphorylation. We detected expression of \u03b2ENaC and \u03b3ENaC subunits in rat PCA by Western blots and immunofluorescence. Inhibition of ENaCs with amiloride, ethyl isopropyl amiloride or benzamil blocked the myogenic response. Moreover, the myogenic response was inhibited in rat PCA transfected with \u03b2ENaC and \u03b3ENaC small interfering RNA. The myogenic response was inhibited by elimination of external Na<jats:sup>+<\/jats:sup>, which was replaced with <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010glucamine. Amiloride and nifedipine inhibited the pressure\u2010induced increase in Ca<jats:sup>2+<\/jats:sup> concentration. Finally, MLC<jats:sub>20<\/jats:sub> increased when the intraluminal pressure was raised, and the pressure\u2010induced increase in MLC<jats:sub>20<\/jats:sub> phosphorylation was inhibited by pretreatment with amiloride, and in arteries transfected with \u03b2ENaC or \u03b3ENaC small interfering RNA. Our results suggest that ENaCs may play an important role as mechanosensitive ion channels initiating pressure\u2010induced myogenic responses in rat PCA.<\/jats:p>","DOI":"10.1113\/expphysiol.2011.062232","type":"journal-article","created":{"date-parts":[[2011,11,17]],"date-time":"2011-11-17T13:06:21Z","timestamp":1321535181000},"page":"544-555","source":"Crossref","is-referenced-by-count":33,"title":["Epithelial Na<sup>+<\/sup> channel proteins are mechanotransducers of myogenic constriction in rat posterior cerebral 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