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Am J Physiol Heart Circ Physiol 279: H1147-H1156, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 3, H1147-H1156, September 2000

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

Carl F. Rothe and Roberto Maass-Moreno

Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, Indiana 46202

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.

vascular capacitance; hepatic venular pressure; servo-null micropressure pipette for pressure; presinusoidal resistance; venoconstriction


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