Articulo
Inhibition of epithelial sodium channel (enac) with amilorideimproves endothelium-derived vasodilation in angiotensin ii(aii)-treated rats
FASEB JOURNAL;
FASEB J
Registro en:
1090757
1090757
0892-6638
Autor
Boric, Mauricio P.
Paz Beltran, Maria
Soto, Nicolas
Figueroa, Xavier F.
Institución
Resumen
ENaC is expressed in the endothelium, and may affect vascular tone, since inhibitors of the mineralocorticoid receptor, ENaC main regulator, produce favorable effects in different types of hypertension, independently of renal effects. We assessed the hypothesis that a moderate activation of the renin-angiotensin-aldosterone system increases ENaC endothelial activity, reducing endothelium-dependent vasodilation probably by modifying the Na/Ca exchanger function. Moderate hypertension was induced in SD rats (100g) with AII infusion (40–200 ng/Kg/min, 2 weeks, osmotic pump). Controls were sham operated. No difference was detected in vivo to the depressor response elicited by bradykinin. In aortic rings from AII-treated rats, phenyleprhrine (PE)-induced constriction was higher and acetylcholine (ACh)-induced relaxation was smaller than control. In AII-treated vessels, ENaC blockade with amiloride (300nM) reduced PE constriction and fully restored the relaxation to ACh, but did not modify endothelium-independent relaxation to isoproterenol. Similarly, amiloride caused significant dilation (22±5%) of isolated, pressurized and perfused skeletal muscle arterioles (~150?m). Amiloride had no effect in arteriolar tone, or aortic responses of control vessels. We conclude that ENaC blockade improves endothelium-dependent relaxation in AII-induced mild hypertensive rats. FONDECYT FONDECYT 25