Source:http://linkedlifedata.com/resource/pubmed/id/16460765
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
15
|
pubmed:dateCreated |
2006-2-27
|
pubmed:abstractText |
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 microM) transiently inhibited Na,K-ATPase activity for 10-15 min. A direct activator of protein kinase A, 8-Br-cAMP (150 and 500 microM), also inhibited, but more rapidly and for a shorter duration. Both DAMGO (1 microM) and Rp-adenosine 3',5'-cyclic monophosphorothioate (500 microM), a protein kinase A-inhibitor, reversed the inhibitory effect of prostaglandin E1. DAMGO alone (1 microM) stimulated Na,K-ATPase activity up to nearly three-fold control activity. The stimulatory action of DAMGO was blocked by cyclosporine A (2 microM), 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 microM). 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.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alprostadil,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, L-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Enkephalin, Ala(2)-MePhe(4)-Gly(5)-,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid, mu,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
0024-3205
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
6
|
pubmed:volume |
78
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1653-61
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:16460765-Alprostadil,
pubmed-meshheading:16460765-Calcium Channels, L-Type,
pubmed-meshheading:16460765-Cell Line, Tumor,
pubmed-meshheading:16460765-Cyclic AMP,
pubmed-meshheading:16460765-Dose-Response Relationship, Drug,
pubmed-meshheading:16460765-Drug Interactions,
pubmed-meshheading:16460765-Enkephalin, Ala(2)-MePhe(4)-Gly(5)-,
pubmed-meshheading:16460765-Enzyme Activation,
pubmed-meshheading:16460765-Enzyme Inhibitors,
pubmed-meshheading:16460765-Humans,
pubmed-meshheading:16460765-Receptors, Opioid, mu,
pubmed-meshheading:16460765-Signal Transduction,
pubmed-meshheading:16460765-Sodium-Potassium-Exchanging ATPase
|
pubmed:year |
2006
|
pubmed:articleTitle |
Modulation of Na, K-ATPase activity by prostaglandin E1 and [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin.
|
pubmed:affiliation |
University of Puerto Rico School of Medicine, Institute of Neurobiology and Department of Pharmacology and Toxicology, San Juan, 00901, Puerto Rico.
|
pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|