Differential effect of taurocholic acid on hepatic arterial resistance vessels and bile flow.

Abstract

The "hepatic arterial buffer response" hypothesis states that the hepatic artery is not controlled by liver parenchymal cell metabolic activity. Bile salts stimulate liver metabolism (elevate bile formation) and dilate the hepatic artery. The present data show that the vascular and metabolic effects in cats anesthetized with pentobarbital sodium are independent. Low doses of taurocholate (1 microM . min-1 . kg-1) produce metabolic but not vascular responses. At higher doses both the hepatic artery and superior mesenteric artery dilate with equal sensitivity. Taurocholate into the portal vein produced elevated bile flow and hepatic arterial dilation; infusion via the hepatic artery resulted in equal metabolic responses but much greater vascular effects. In addition, the time course of onset and termination of the metabolic and vascular responses supports the conclusion that the effects of taurocholic acid on hepatic bile flow and hepatic arterial flow are independent actions. This adds further support for the hepatic arterial buffer response being controlled by factors other than local hepatic metabolic demands.