Keishi Yamauchi*, Koji Nakajima, Sachiko Ikeo, Yoshihiro Nishimura, Mitsuhisa Komatsu, Toru Aizawa and Kiyoshi Hashizume
Department of Aging Medicine and Geriatrics, Shinshu University School of Medicine, Matsumoto 390-8621, Japan
*Corresponding author. FAX: +81-263-37-2710, E-mail: email@example.com
Abstract: Effects of nipradilol, a b-adrenoceptor blocker with a nitroxy moiety, on phosphoenolpyruvate carboxykinase (PEPCK) gene transcription were examined using a rat hepatoma cell line, H4IIE cells. Dexamethasone was employed as an enhancer of PEPCK gene transcription. Nipradilol, but not timolol (a b-blocker without a nitroxy moiety), attenuated PEPCK gene transcription both in the control and the dexamethasone-treated cells. The effects of nipradilol were eradicated by methylene blue (an inhibitor of cellular guanylate cyclase). Nipradilol is a unique b-blocker that suppresses PEPCK gene transcription in hepatocytes likely through liberation of nitric oxide and resultant activation of guanylate cyclase.
Keywords: Dexamethasone, Phosphoenolpyruvate carboxykinase, Nipradilol
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