Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor.

Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor. Research Abstract Details 

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Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor. Abstract Text:

Takahiro Horinouchi,Yumie Miyake,Tadashi Nishiya,Arata Nishimoto,Shoko Yorozu,Atsushi Jinno,Emi Kajita,Soichi Miwa,Takahiro Horinouchi,Yumie Miyake,Tadashi Nishiya,Arata Nishimoto,Shoko Yorozu,Atsushi Jinno,Emi Kajita,Soichi Miwa,

The mechanism for noradrenaline (NA)-induced increases in intracellular Ca(2+) concentration ([Ca(2+)](i)) and physiological significance of Na(+) influx through receptor-operated channels (ROCs) and store-operated channels (SOCs) were studied in Chinese hamster ovary (CHO) cells stably expressing human alpha(1A)-adrenoceptor (alpha(1A)-AR). [Ca(2+)](i) was measured using the Ca(2+) indicator fura-2. NA (1 microM) elicited transient and subsequent sustained [Ca(2+)](i) increases, which were inhibited by YM-254890 (G(alphaq/11) inhibitor), U-73122 (phospholipase C (PLC) inhibitor), and bisindolylmaleimide I (protein kinase C (PKC) inhibitor), suggesting their dependence on G(alphaq/11)/PLC/PKC. Both phases were suppressed by extracellular Ca(2+) removal, SK&F 96365 (inhibitor of SOC and nonselective cation channel type-2 (NSCC-2)), LOE 908 (inhibitor of NSCC-1 and NSCC-2), and La(3+) (inhibitor of transient receptor potential canonical (TRPC) channel). Reduction of extracellular Na(+) and pretreatment with KB-R7943, a Na(+)/Ca(2+) exchanger (NCX) inhibitor, inhibited both phases of [Ca(2+)](i) increases. These results suggest that 1) stimulation of alpha(1A)-AR with NA elicits the transient and sustained increases in [Ca(2+)](i) mediated through NSCC-2 that belongs to a TRPC family; 2) Na(+) influx through these channels drives NCX in the reverse mode, causing Ca(2+) influx in exchange for Na(+) efflux; and 3) the G(alphaq/11)/PLC/PKC-dependent pathway plays an important role in the increases in [Ca(2+)](i).

Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor. Publishing Authors By Initials

T Horinouchi,Y Miyake,T Nishiya,A Nishimoto,S Yorozu,A Jinno,E Kajita,S Miwa,T Horinouchi,Y Miyake,T Nishiya,A Nishimoto,S Yorozu,A Jinno,E Kajita,S Miwa,

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Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of pharmacological sciences

VOLUME: 105

Page Numbers: 103-11

Journal Abbreviation: J. Pharmacol. Sci.

ISSN: 1347-8613

DAY: 8

MONTH: 09

YEAR: 2007

Characterization of noradrenaline-induced increases in intracellular Ca2+ levels in Chinese hamster ovary cells stably expressing human alpha1A-adrenoceptor. Information

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LANGUAGE: eng

NlmUniqueID: 101167001

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AFFILIATION: Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan.

Country: Japan

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MEDLINETA: J Pharmacol Sci

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