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Am J Physiol Lung Cell Mol Physiol (February 22, 2002). doi:10.1152/ajplung.00436.2001
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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00436.2001
Submitted on November 8, 2001
Accepted on February 14, 2002

Alkalosis stimulates endothelial nitric oxide synthase in cultured human pulmonary arterial endothelial cells

Shiro Mizuno1*, Yoshiki Demura1, Shingo Ameshima1, Seitaro Okamura1, Isamu Miyamori1, and Takeshi Ishizaki1

1 Third Department of Internal Medicine, Fukui Medical University, Fukui, Yoshida-gun, Japan

* To whom correspondence should be addressed. E-mail: shirotan{at}qf6.so-net.ne.jp.

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 - 8.0). eNOS activity was found to increase with alkalization and decrease with acidification, while Ca2+ uptake into HPAEC increased with alkalization. The addition of 3',4'-dichlorobenzamil hydrochloride, an inhibitor of the Na+/Ca/2+ exchanger (NCX), prevented the increase of eNOS activity with alkalosis. Exposure to alkalosis and acidosis increased eNOS and NCX mRNA levels. These results suggested that an elevation of extracellular pH activates eNOS via the influx of extracellular Ca2+, and that NCX also regulate eNOS activity during alkalosis. Further, NCX may have a tight interaction with eNOS at the level of transcription, and might affect pulmonary circulation during alkalosis and acidosis.




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