AIM To study hepatic vasoconstriction and glucose release induced by angiotensin(Ang)Ⅱ or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat(SHR).METHODS Isolated liver perfusion was performed following portal vein and vena cava cannulation; AngⅡ or epinephrine(Epi) was injected in bolus and portal pressure monitored; glucose release was measured in perfusate aliquots. RESULTS The portal hypertensive response(PHR) and the glucose release induced by AngⅡ of L-NAME were similar to normal rats(WIS). On the other hand, the PHR inducedby Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by AngⅡ was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar. CONCLUSION AngⅡ and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by AngⅡ; the diminished glucose release induced by AngⅡ in SHR is not related to glycogen content. AIM To study hepatic vasoconstriction and glucose release induced by angiotensin (Ang) II or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat (SHR). METHODS Isolated liver perfusion was performed following portal vein and vena cava cannulation; Ang II or epinephrine (Epi) RESULTS The portal hypertensive response (PHR) and the glucose release induced by AngⅡ of L-NAME were similar to normal rats (WIS). On the other hand, the PHR induced by Epi in L-NAME was higher than the glucose release was lower compared to WIS. However, the similar glycogen content, glucose release induced by AngⅡ was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar. CONCLUSION Ang Ⅱ and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems t o be involved in the hepatic effects induced by Epi but not by Ang II; the diminished glucose release induced by Ang II in SHR is not related to glycogen content.