Active and passive liver microvascular responses from angiotensin, endothelin, norepinephrine, and vasopressin

Abstract

Vasoconstrictor agents may induce a decrease in hepatic vascular volume passively, by decreasing distending pressure, or actively, by stimulating contractile elements of capacitance vessels. Hepatic venular resistance was estimated in anesthetized rabbits from hepatic venular pressure (Pμhv; by servo-null micropipette), inferior vena cava pressure, and total hepatic blood flow (Fhv; by ultrasound flow probe). Changes in liver volume were estimated from measures of liver lobe thickness. Angiotensin (ANG) II, endothelin (ET)-1, norepinephrine (NE), and vasopressin (VP) were infused into the portal vein at a constant rate for 5 min. We conclude that ANG II and NE induced active constriction of hepatic capacitance vessels, because the liver lobe thickness decreased significantly even though Pμhv and portal venous distending pressure (Ppv) increased. All four agents increased splanchnic and hepatic venous resistances in similar proportions. With VP, Pμhv and Ppv decreased, but with ET-1, Pμhv and Ppv increased. However, lobe thickness was not significantly changed by either drug during the infusion compared with the 2-min control period. Thus VP and ET-1 have only minor effects on hepatic capacitance vessels. ET-1, at 0.04 μg · min−1 · kg body wt−1, caused an increase in systemic arterial blood pressure, but erythrocyte movement through the sinusoids in some animals stopped.