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In Comparison of Sodium Pump Regulation between Thoracic Aortas and Mesenteric Arteries in Rats
並列摘要
Background: The electrogenic sodium pump (Na^+-K^+-ATPase) contributes to the maintenance of intracellular ionic concentration, and thus, controls membrane potential and vascular tone. Methods: We compared the regulation of Na^+-K^+-ATPase activity between the thoracic aorta and the mesenteric artery in the rat by removing the endothelium or changing the levels of cyclic AMP/protein kinase A (cAMP/PKA), protein kinase C (PKC) and nitric oxide/cyclic GMP/protein kinase G (NO/cGMP/PKG). The potassium-induced relaxation in arteries incubated in K^+-free solution was used as a functional indicator of Na^+-K^+-ATPase activity for ouabain abolished the potassium-induced relaxation in these preparations. Results: Potassium-induced relaxations after removal of the endothelium were moderately blunted in these arteries. In the presence of N^ω-nitro-L-arginine methyl ester, but not indomethacin, the potassium-induced relaxation was also inhibited in these preparations. Similar inhibitions of potassium-induced relaxations were observed in aortas, but not in mesenteric arteries, treated with 8-bromo-cAMP or phorbol 12-myristate 13-acetate (PMA). In contrast to 8-bromo-cAMP and PMA, 8-bromocGMP enhanced the potassium-induced relaxation in both preparations. In addition, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one attenuated those relaxations in both preparations whereas sodium nitroprusside enhanced that relaxation in mesenteric arteries only. Conclusions: These results suggest that the endothelium is a functional stimulator of the Na^+-K^+-ATPase activity in both vascular beds. In addition, cAMP/PKA and PKC pathways play a more important role in the aorta than in the mesenteric artery while the NO/cGMP pathway stimulates that pump in both vascular beds. It is likely that in the mesenteric artery exogenous NO may act on rather than cGMP (e.g., potassium channels) to activate the sodium pump in the mesenteric artery.
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