Regulation of Na(superscript +)-K(superscript +)-ATPase in Rat Aortas: Pharmacological and Functional Evidence

Kao-Hsiang Chen；Shiu-Jen Chen；Chin-Chen Wu

sodium pump ； cAMP-PKA ； PKC ； NO-cGMP ； rat aortas

The Chinese Journal of Physiology

48卷2期（2005 / 06 / 01）

86 - 92

英文

Electrogenic sodium pump (Na(superscript +)-K(superscript +)-ATPase) maintains intracellular ionic concentration and controls membrane potential. Therefore, we analyzed the modulation of Na(superscript +)-K(superscript +)-ATPase activity by the endothelium, cyclic AMP-protein kinase A (cAMP-PKA), protein kinase C (PKC) and nitric oxide-cyclic GMP-protein kinase G (NO-cGMP-PKG) in isolated rat thoracic aortas. The potassium-induced relaxation in arteries incubated in K-free solution was used as a functional indicator of Na(superscript +)-K(superscript +)-ATPase activity for ouabain abolished the potassium-induced relaxation in rat aortas. Potassium-induced relaxations after removal of the endothelium were moderately blunted in these preparations. In the presence of N(superscript ω)-nitro-L-arginine methyl ester, but not indomethacin, the potassium-induced relaxation was also inhibited. Similar inhibitions of potassium-induced relaxations were observed in aortas treated with 8-bromo-cAMP and phorbo1 12-myristate 13-acetate (PMA). Although inhibitors of PKA and PKC individually did not affect the potassium-induced relaxation, the combination of both inhibitors significantly potentiated that relaxation. In contrast to 8-bromo-cAMP and PMA, 8-bromo-cGMP enhanced the potassium-induced relaxation whereas 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one attenuated that relaxation. These results suggested that endothelium is a functional stimulator of the Na(superscript +)-K(superscript +)-ATPase activity. In addition, cAMP-PKA and PKC pathways inhibited the sodium pump while the NO-cGMP pathway stimulated this pump in the vascular bed.