Venlafaxine and atenolol disrupt epinephrine-stimulated glucose production in rainbow trout hepatocytes

摘要: The beta-blocker atenolol (ATEN), and the selective serotonin norepinephrine reuptake inhibitor, venlafaxine (VEN) are found in municipal wastewater effluents, but little is known about effect of these pharmaceuticals on aquatic animals. We tested hypothesis that VEN ATEN disrupt acute stress mediated glucose production fish liver. To this end, rainbow trout (Oncorhynchus mykiss) hepatocytes were exposed vitro to different concentrations (0, 0.1, 10, 1000 nM) or response either cortisol epinephrine (two key hormones) was ascertained. Both did not affect unstimulated (100 ng/mL)-stimulated release over a 24 h period. (3 h) by isolated suspension also modified ATEN, while reduced basal release. However, even at concentration as low 0.01 nM completely abolished (1 μM)-induced hepatocytes. Interestingly, suppressed epinephrine-induced only higher nM). Neither nor significantly impacted 8-bromo-cAMP (cAMP analogue) glucagon (a metabolic hormone increases production) stimulation. attenuated increase transporter 2 (GLUT2) mRNA abundance Taken together, our results suggest impact involves inhibition β-adrenoceptor signaling Overall, beta-blockers may adaptive secondary stressor trout.