{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:48:32Z","timestamp":1790617712295,"version":"4.1.0"},"reference-count":32,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2002,7,1]]},"abstract":"<jats:p> To investigate the effect of extracellular pH on endothelial nitric oxide synthase (eNOS) in human pulmonary arteries, we measured eNOS activity and expression as well as some ion channels in human pulmonary arterial endothelial cells (HPAEC) exposed to various pH levels (6.6\u20138.0). eNOS activity was found to increase with alkalization and decrease with acidification, while Ca<jats:sup>2+<\/jats:sup> uptake into HPAEC increased with alkalization. The addition of 3\u2032,4\u2032-dichlorobenzamil hydrochloride, an inhibitor of the Na<jats:sup>+<\/jats:sup>\/Ca<jats:sup>2+<\/jats:sup> exchanger (NCX), prevented the increase of eNOS activity with alkalosis. Exposure to alkalosis and acidosis increased eNOS and NCX mRNA levels. These results suggest that an elevation of extracellular pH activates eNOS via the influx of extracellular Ca<jats:sup>2+<\/jats:sup> and that NCX also regulates eNOS activity during alkalosis. Furthermore, NCX may have a tight interaction with eNOS at the level of transcription and might affect pulmonary circulation during alkalosis and acidosis. <\/jats:p>","DOI":"10.1152\/ajplung.00436.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T15:17:43Z","timestamp":1425395863000},"page":"L113-L119","source":"Crossref","is-referenced-by-count":27,"title":["Alkalosis stimulates endothelial nitric oxide synthase  in cultured human pulmonary arterial endothelial cells"],"prefix":"10.1152","volume":"283","author":[{"given":"Shiro","family":"Mizuno","sequence":"first","affiliation":[{"name":"Third Department of Internal Medicine, Fukui Medical University, Fukui 910-1193, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiki","family":"Demura","sequence":"additional","affiliation":[{"name":"Third Department of Internal Medicine, Fukui Medical University, Fukui 910-1193, 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