Mechanisms in the pressor effects of hepatic portal venous fatty acid infusion

Mechanisms in the presser effects of hepatic portal venous fatty acid infusion. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): E2324-R330, 1997.-Portal venous infusion of oleate solution has presser effects. We have examined efferent mechanisms, measured the response to sustained infusion, and determined the effect of linoleate. Eight conscious animals received concurrent infusions of prazosin or vehicle with portal venous infusion of oleate. Oleate alone increased mean arterial pressure from 109.0 +/- 4.1 to 123.0 +/- 5.8 mmHg (P = 0.02), whereas no increase in blood pressure occurred when oleate was infused with prazosin. In 10 rats, concurrent infusion of losartan had no effect on the presser activity of portal oleate infusion. Twenty-two animals received portal oleate or vehicle as a continuous infusion far 7 days. Mean arterial pressure (126.1 +/- 2.0 vs. 107.8 +/- 2.6 mmHg, P < 0.001) and heart rate (383 +/- 5 vs. 366 +/- 5, P = 0.0257) were increased in oleate-infused animals. No differences in plasma fatty acids, glucose, insulin, presser hormones, liver enzymes, or in vitro arterial presser responsiveness were observed. Portal venous infusion of linoleate increased arterial pressure by 12.2 +/- 3.2 mmHg (P = 0.033). These results indicate that alpha-adrenergic activity is necessary for the acute presser effects of portal oleate, that sustained portal oleate infusion results in persistent blood pressure elevation, and that other long-chain fatty acids besides oleate have presser effects.