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Regulation of endothelin‐1 action on the perfused rat liver
Author(s) -
Tran-Thi Thuy-Anh,
Kawada Norifumi,
Decker Karl
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80544-5
Subject(s) - glycogenolysis , endocrinology , iloprost , nitric oxide , medicine , protein kinase c , chemistry , prostacyclin , endothelin receptor , contraction (grammar) , extracellular , endothelin 1 , endogeny , signal transduction , prostaglandin , biology , biochemistry , glycogen , receptor
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 Ca 2+ 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 I 2 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.