Calcium‐activated membrane depolarization via modulation of chloride efflux from parietal cells during gastrin stimulation

FEBS Letters

Tsunoda, Yasuhiro¹  Matsumiya, Hidemi¹ 

[1] Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo 060, Hokkaido, Japan

关键词: Gastrin;    Ca2+ release;    Depolarization;    Cl− efflux;    (Parietal cell;    Guinea pig);    fura-2;    1-(2-(5′-carboxyoxazol-2′-yl)-6-aminobenzofuran -5-oxy)-2-(2′-amino-5′-methylphenoxy-ethane-N;    N;    N′;    N′-tetraacetic acid;    BAPTA;    1;    2-bis(o - aminophenoxy)ethane - N;    N;    N′;    N′ - tetraacetic acid;    diS-C3-(5);    3;    3′-dipropylthiodicarbocyanine;    Mops;    3-(N-morpholino)propanesulfonic acid;    quin-2;    2-(2-amino-5-methylphenoxy)methyl-6-methoxy-8-aminoquinoline-N;    N;    N′;    N′-tetraacetic acid;   

DOI  :  10.1016/0014-5793(87)80209-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

In the isolated parietal cell the following observations were made: gastrin led to an increase in cytoplasmic free Ca²⁺ concentration ([Ca²⁺]_i) even in the absence of medium Ca²⁺ and to transient membrane depolarization in both the absence of the medium Ca²⁺ and the fura-2-loaded cell. The incorporated Ca²⁺ chelator BAPTA inhibited the gastrin-induced membrane depolarization. The magnitude of depolarization caused by gastrin was unchanged on removal of medium Na⁺. Furosemide but not tetraethylammonium inhibited the gastrin-induced depolarization. The results suggest that the Ca²⁺ released from the store(s) induces membrane depolarization, possibly via modulation of a Cl⁻ efflux across the luminal surface during gastrin stimulation.

【 授权许可】

Unknown