Background: Hyperlipidemia has been implicated in the pathogenesis of hypertension and cardiovascular diseases. However, the direct role and decay pattern of hypertriglyceridemia in regulation of blood pressure remain undefined. Methods: This study examined the pressor response to acute hypertriglyceridemia by infusing lipofundin (a 20% triglyceride emulsion) and its decay pattern under basal glucose and insulin conditions. Rats were randomly assigned into two groups of eight rats, and lipofundin or saline was infused during the test period. The experiment contained a 30 min basal period, followed by a 120 min test period and a 90 min off period. After the basal period, somatostatin (1.3μg..kg-1.min-1) combined with regular insulin (0.6 mU.kg-1.min-1) and a variable glucose infusion were given to keep insulin and glucose at basal levels throughout the experiment. Results: In the lipid-infused rats, lipofundin (1.2 ml.kg-1.hr-1) was given to create hypertriglyceridemia during the test period, which dropped promptly and returned to basal level by 60 min in the off period. Mean arterial pressure (MAP) was significantly increased for 60 min after lipofundin infusion and reached a plateau at 90 min postinfusion. This elevated MAP was sustained even after the lipofundin infusion was discontinued. Plasma NOx (the sum of NO2 and NO3) levels were significantly elevated during the test period and increased further in the off period. In control rats, MAP, HR, and NOx levels were not altered throughout the study. Conclusions: These findings demonstrate that hyperlipidemia, especially elevated plasma triglyceride levels, can induce a long-lasting pressor response in rats. Our results also imply that the pressor effect of hypertriglyceridemia-induced attenuation of NO production may not be of importance in this model.