Peroxisome Proliferator–Activated Receptor γ Regulates Angiotensin II–Stimulated Phosphatidylinositol 3-Kinase and Mitogen-Activated Protein Kinase in Blood Vessels In Vivo

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2006-01, Vol.47 (1), p.102-108
• Main Authors: Benkirane, Karim, Viel, Émilie C, Amiri, Farhad, Schiffrin, Ernesto L
• Format: Article
• Language: English
• Subjects: Angiotensin II - pharmacology; Animals; Aorta - enzymology; Aorta - metabolism; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - drug effects; Blood vessels and receptors; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Fundamental and applied biological sciences. Psychology; Male; Medical sciences; Mesenteric Arteries - enzymology; Mesenteric Arteries - metabolism; Mitogen-Activated Protein Kinases - metabolism; Phosphatidylinositol 3-Kinases - metabolism; PPAR gamma - metabolism; PPAR gamma - physiology; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1 - metabolism; Signal Transduction - drug effects; Thiazolidinediones - pharmacology; Vasoconstrictor Agents - pharmacology; Vasodilator Agents - pharmacology; Vertebrates: cardiovascular system
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.0000196728.05488.c3

Angiotensin (Ang) II is implicated in hypertension, vascular remodeling, and insulin resistance. Peroxisome proliferator–activated receptor (PPAR) γ activators increase insulin sensitivity and improve Ang II–induced vascular remodeling. We evaluated the effects of the PPAR-γ activator rosiglitazone on Ang II signaling in aorta and mesenteric arteries. Rats received Ang II by subcutaneous infusion and/or rosiglitazone per os for 7 days. Blood pressure rise in Ang II–infused rats was attenuated by rosiglitazone. Ang II significantly increased Ang II type 1 receptor expression in the mesenteric arteries (P