Abstract
1The hepatic portal vein of the anaesthetized dog was cannulated and perfused with blood derived from the cannulated superior mesenteric vein. 2The portal vein was perfused at constant flow, the hepatic portal venous pressure being monitored continuously together with the inferior vena caval pressure. From these measurements, the hepatic portal venous vascular resistance was calculated. 3Noradrenaline and adrenaline were injected intraportally in graded doses which caused dose-dependent increases in the hepatic portal vascular resistance. At all doses, adrenaline was significantly (P<0.05) more potent than noradrenaline. 4Intraportal injections of vasopressin caused reductions in calculated hepatic portal venous vascular resistance in most experiments; these effects were dose-dependent. 5No tachyphylaxis to the effects of noradrenaline, adrenaline or vasopressin was observed. 6Intraportal injections of angiotensin caused dose-dependent increases in calculated hepatic portal vascular resistance up to 5 μg; thereafter larger doses caused smaller increases in portal resistance. 7Repeated intraportal injections of angiotensin revealed the existence of tachyphylaxis in the hepatic portal vascular bed. 8Intraportal infusions of angiotensin caused rises in calculated hepatic portal vascular resistance from which there was almost complete ‘escape’ despite the continued infusions. Infusions of noradrenaline which caused similar rises in calculated portal vascular resistance did not exhibit equivalent degrees of ‘escape’. 9The development of tachyphylaxis explains the fact that doses of 10 and 20 μg of angiotensin injected after 5 μg doses produced smaller effects. If a much longer time interval was allowed between injections (30 min), the dose-response curve to angiotensin had a sigmoid shape. 10These findings are discussed with respect to their possible importance in the functional status of the hepatic portal vascular bed in this species.