Regulation of endothelin‐1 action on the perfused rat liver

FEBS Letters

Kawada, Norifumi¹  Tran-Thi, Thuy-Anh¹  Decker, Karl¹ 

[1] Biochemisches Institut der Albert-Ludwigs-Universität, Hermann-Herder-Str. 7, D-7800 Freiburg i.Br., Germany

关键词: Calcium ion;    Eicosanoid;    Nitric oxide;    Protein kinase C;    Vasoconstriction;    ET-1;    endothelin-1;    NO;    nitric oxide;    PG;    prostaglandin;    sin-1;    3-morpholino-sydnoimine-N-ethylcarbamide;    SNP;    sodium nitroprusside;   

DOI  :  10.1016/0014-5793(93)80544-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Endothelin-1 (ET-1) was found to be a very potent stimulus for contraction and glycogenolysis in the perfused rat liver. At 1 nM it caused a dramatic increase in portal pressure of 22.1 ± 2.7 cm water and enhanced the glucose output up to 3-fold. Extracellular Ca²⁺ and protein kinase C were involved in the signal transduction of ET-1. ET-1 action does not seem to be mediated by endogenous eicosanoids. The effects of ET-1 were significantly reduced in the presence of 1 μM Iloprost, a prostaglandin I₂ analogue, or by 100 μM sin-1, a nitric oxide donor. In cultured hepatocytes, glycogenolysis was also stimulated by ET-1 although to an extent too small to explain the high glucose output found in the perfused liver.

【 授权许可】

Unknown