title: Effect of short-term cyclic stretch on sodium pump activity in aortic smooth muscle cells.
abstract: We previously demonstrated that expression of both the alpha1- and alpha2-subunits of Na+-K+-ATPase is elevated after a 2- to 4-day cyclic stretch in aortic smooth muscle cells. In this study, we determined the effect of short-term (2-30 min) cyclic stretch on the activity of the Na pump and investigated possible mechanisms that may be involved in the action of stretch. Na pump activity was significantly increased above the baseline activity between 2 and 30 min of stretch. This effect of stretch was reversible within 1 h. Intracellular Na was also elevated at corresponding time points. Blocking the entry of Na with Gd and amiloride did not affect the stretch-induced increase in Na pump activity. Inhibition of protein kinase A (PKA) activity attenuated the effect of stretch on the Na pump. Furthermore, inhibition of polymerization of actin and phosphatidylinositol 3-kinase (PI3K) activity prevented the action of stretch on Na pump activity. We conclude that the stimulation of the Na pump in response to cyclic stretch requires the integrity of the actin cytoskeleton as well as the activity of PI3K, which has a role in intracellular vesicular trafficking. PKA may also be involved in this effect of stretch on Na pump.
authors.affiliation: Department of Pharmacology and Experimental Therapeutics, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA. emize@lsuhsc.edu
authors.forename: E
authors.initials: E
authors.lastname: Songu-Mize
authors.forename: N
authors.initials: N
authors.lastname: Sevieux
authors.forename: X
authors.initials: X
authors.lastname: Liu
authors.forename: M
authors.initials: M
authors.lastname: Jacobs
mesh_terms: D000199:Actins / Q000378:metabolism; D000584:Amiloride / Q000494:pharmacology; D000730:Androstadienes / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000166:cytology; D002478:Cells, Cultured; D003078:Colchicine / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000378:metabolism; D004232:Diuretics / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005682:Gadolinium / Q000494:pharmacology; D007546:Isoquinolines / Q000494:pharmacology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000201:enzymology*; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013314:Stress, Mechanical; D013449:Sulfonamides; D000077191:Wortmannin
chemical_list: D000199:Actins; D000730:Androstadienes; D004232:Diuretics; D004791:Enzyme Inhibitors; D007546:Isoquinolines; D019384:Nucleic Acid Synthesis Inhibitors; D000081082:Phosphoinositide-3 Kinase Inhibitors; D013449:Sulfonamides; D015638:Cytochalasin D; D000584:Amiloride; D005682:Gadolinium; D017868:Cyclic AMP-Dependent Protein Kinases; D000254:Sodium-Potassium-Exchanging ATPase; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D003078:Colchicine; D000077191:Wortmannin