title: Regulation of endothelin-1 action on the perfused rat liver.
abstract: 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 microM Iloprost, a prostaglandin I2 analogue, or by 100 microM 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.
authors.affiliation: Biochemisches Institut, Albert-Ludwigs-Universität, Freiburg, Germany.
authors.forename: T A
authors.initials: TA
authors.lastname: Tran-Thi
authors.forename: N
authors.initials: N
authors.lastname: Kawada
authors.forename: K
authors.initials: K
authors.lastname: Decker
mesh_terms: D000818:Animals; D001646:Bile / Q000502:physiology; D002118:Calcium / Q000494:pharmacology; D002478:Cells, Cultured; D016232:Endothelins / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D007700:Kinetics; D008099:Liver / Q000098:blood supply* / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism / Q000494:pharmacology; D010477:Perfusion; D017082:Portal Pressure; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D014661:Vasoconstriction
chemical_list: D016232:Endothelins; D009569:Nitric Oxide; D006003:Glycogen; D011464:Epoprostenol; D011493:Protein Kinase C; D005947:Glucose; D002118:Calcium; D007213:Indomethacin