Physiological regulation of the hepatic circulation

Liver blood flow is determined at normal arterial pressure by 1) the hepatic arterial vascular resistance, 2) the inflow resistance to the preportal vascular beds, 3) the intrahepatic portal venous vascular resistance. Hepatic arterial vascular resistance and therefore blood flow are regulated by relatively weak intrinsic as well as by extrinsic mechanisms. The principal extrinsic mechanisms include the sympathetic vasoconstrictor innervation and epinephrine, whereas the roles of the vasodilator gastrointestinal and pancreatic hormones, and autacoids released from the gastrointestinal tract, remain to be established convincingly. Intrahepatic portal vascular resistance is not significantly controlled by intrinsic mechanisms, and responses to extrinsic mechanisms may be directed principally toward maintenance of portal venous pressure. Two aspects of liver blood flow are discussed in particular detail. First, hormones or drug introduced into one inflow to the liver (e.g., the portal vein) alter the vascular resistance not only of that circuit, but also of the other inflow circuit (hepatic arterial) by a transhepatic mechanism that does not depend on recirculation of the hormone or drug. Second, glucagon, but not other polypeptide vasodilator hormones, prevents hepatic arterial vasoconstriction due to stimuli that include sympathetic nerve activation. This effect occurs at portal or arterial glucagon concentrations close to the pathophysiological range.