Regulation of endothelin‐1 action on the perfused rat liver

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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 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.