کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2554798 | 1124992 | 2006 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Modulation of Na, K-ATPase activity by prostaglandin E1 and [d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin Modulation of Na, K-ATPase activity by prostaglandin E1 and [d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin](/preview/png/2554798.png)
Adenylyl cyclase is activated by prostaglandin E and inhibited by mu-opioids. Since cAMP-related events influence the activity of the Na Pump and its biochemical correlate Na,K-ATPase in many systems, we tested the hypothesis that prostaglandin E1 and [d-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO), a mu-opioid agonist, have opposing actions on Na,K-ATPase activity. Studies were conducted with alamethicin-permeabilized SH-SY5Y human neuroblastoma cells. Prostaglandin E1 (1 μM) transiently inhibited Na,K-ATPase activity for 10–15 min. A direct activator of protein kinase A, 8-Br-cAMP (150 and 500 μM), also inhibited, but more rapidly and for a shorter duration. Both DAMGO (1 μM) and Rp-adenosine 3′,5′-cyclic monophosphorothioate (500 μM), a protein kinase A-inhibitor, reversed the inhibitory effect of prostaglandin E1. DAMGO alone (1 μM) stimulated Na,K-ATPase activity up to nearly three-fold control activity. The stimulatory action of DAMGO was blocked by cyclosporine A (2 μM), an inhibitor of calcineurin, and was dependent on Ca2+ entry through nifedipine-sensitive Ca2+ channels. In the presence of 1 mM EGTA, DAMGO inhibited Na,K-ATPase activity. DAMGO-induced inhibition was blocked by the inositol 1,4,5-trisphosphate receptor antagonist xestospongin C (1 μM). Na,K-ATPase is poised to modulate neuronal excitability through its roles in maintaining the membrane potential and transmembrane ion gradients. The differential effects of prostaglandin E1 and opioids on Na,K-ATPase activity may be related to their actions in hyperalgesia.
Journal: Life Sciences - Volume 78, Issue 15, 6 March 2006, Pages 1653–1661