ALPHA-ADRENERGIC RECEPTORS MEDIATE THE HYPERTRIGLYCERIDEMIA INDUCED BY ENDOTOXIN, BUT NOT TUMOR-NECROSIS-FACTOR, IN RATS

We assessed the role of catecholamines in mediating the hypertriglycer idemia induced by lipopolysaccharide (LPS) or tumor necrosis factor-al pha (TNF alpha) in rats by employing specific adrenoreceptor antagonis ts. Pretreatment with phentolamine, an a-antagonist, but not propranol ol, a beta-antagonist, suppressed the hypertriglyceridemia induced by either low dose LPS (100 ng/100 g BW) or high dose LPS (50 mu g/ 100 g BW). Prazosin, an alpha(1)-selective antagonist, significantly suppre ssed the low dose LPS-induced hypertriglyceridemia by inhibiting hepat ic triglyceride secretion, but did not affect the increase in lipolysi s. In contrast, yohimbine, an alpha(2)-selective antagonist, partially suppressed the high dose LPS-induced hypertriglyceridemia by inhibiti ng the decrease in postheparin lipoprotein lipase activity. Treatment with phentolamine and propranolol did not affect the hypertriglyceride mia induced by TNF alpha. In summary, these findings suggest that cate cholamines via alpha-adrenergic, but not beta-adrenergic, receptors ar e mediators of the hypertriglyceridemia induced by either low or high dose LPS in rats. alpha(1)-Adrenergic receptors are involved in mediat ing the increased hepatic triglyceride secretion induced by low dose L PS, whereas alpha(2)-adrenergic receptors are involved in mediating th e decrease in lipoprotein lipase activity induced by high dose LPS. Th e hypertriglyceridemia induced by either low or high dose LPS may be r egulated by a mechanism unrelated to TNF alpha in rats.