Endothelial Epithelial Sodium Channel Inhibition Activates Endothelial Nitric Oxide Synthase via Phosphoinositide 3-Kinase/Akt in Small-Diameter Mesenteric Arteries

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2009-06, Vol.53 (6), p.1000-1007
• Main Authors: Pérez, Francisco R., Venegas, Fabiola, González, Magdalena, Andrés, Sergio, Vallejos, Catalina, Riquelme, Gloria, Sierralta, Jimena, Michea, Luis
• Format: Article
• Language: English
• Subjects: Amiloride - analogs & derivatives; Amiloride - pharmacology; Analysis of Variance; Animals; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Flow Velocity; Blotting, Western; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Epithelial Sodium Channels - drug effects; Epithelial Sodium Channels - metabolism; Immunohistochemistry; In Situ Hybridization; Male; Medical sciences; Mesenteric Arteries - drug effects; Mesenteric Arteries - physiology; Models, Animal; Nitric Oxide - metabolism; Nitric Oxide Synthase - metabolism; Phosphatidylinositol 3-Kinases - metabolism; Phosphorylation; Probability; Random Allocation; Rats; Rats, Sprague-Dawley
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/HYPERTENSIONAHA.108.128520

Recent studies have shown that the epithelial sodium channel (ENaC) is expressed in vascular tissue. However, the role that ENaC may play in the responses to vasoconstrictors and NO production has yet to be addressed. In this study, the contractile responses of perfused pressurized small-diameter rat mesenteric arteries to phenylephrine and serotonin were reduced by ENaC blockade with amiloride (75.1±3.2% and 16.9±2.3% of control values, respectively; P