Noradrenaline and ATP decrease the secretion of triglyceride and apoprotein B from perfused rat liver.

Abstract

To explore the role of hepatic sympathetic nerves on the secretion of very low density lipoprotein (VLDL), the effects of sympathetic neurotransmitters, noradrenaline and ATP, on the secretion of triglyceride and apoprotein B (ApoB) from the liver were studied using rat liver perfused in situ with recirculation. During liver perfusion with physiological medium, the amount of triglyceride in the perfusate was increased linearly for up to 120 min. The addition of noradrenaline to the perfusion medium at a final concentration of 1 muM increased the portal pressure and suppressed the secretion of triglyceride to about 60% of control without an increase in free fatty acid production. The administration of ATP increased the portal pressure with kinetics different from those induced by noradrenaline, but suppressed the triglyceride secretion to an extent similar to that induced by noradrenaline. The suppressive effect of noradrenaline on triglyceride secretion was mimicked by an alpha-adrenoceptor agonist, phenylephrine, and was retained after the haemodynamic changes were prevented by sodium nitroprusside. The secretion of ApoB from the perfused liver was also inhibited by noradrenaline or ATP to about 70% of control. However, hepatic levels of mRNA for ApoB were not significantly altered by noradrenaline and ATP. Since ApoB is the major apoprotein in VLDL, these results suggest that the sympathetic neurotransmitters noradrenaline and ATP suppress the secretion of ApoB-containing lipoprotein including VLDL from the liver, probably acting on post-transcriptional processes.