Endogenous Angiotensin II Produced by Endothelium Regulates Interleukin-1 beta-Stimulated Nitric Oxide Generation in Rat Isolated Vessels

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 30; no. 5; pp. 1191 - 1197
• Main Authors: Monton, Mercedes, Lopez-Farre, Antonio, Mosquera, Juan R, de Miguel, Sanchez Lourdes, Garcia-Duran, Margarita, Sierra, Maria P, Bellver, Teresa, Rico, Luis, Casado, Santos
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.11.1997; Hagerstown, MD Lippincott
• Subjects: Biological and medical sciences; Blood vessels and receptors; Fundamental and applied biological sciences. Psychology; Vertebrates: cardiovascular system; Rat; Enzyme; Cytokine; Peptide hormone; Rodentia; Interleukin 1β; In vitro; Nitric-oxide synthase; Endothelium; Renin angiotensin system; Vertebrata; Regulation(control); Mammalia; Endogenous; Blood vessel; Animal; Nitric oxide; Circulatory system; Oxidoreductases; Angiotensin II
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.30.5.1191

The endothelium is a source of several factors that regulate vascular functions. Angiotensin II is one of the main active factors released by the endothelium. The aim of the present work was to analyze the role of angiotensin II released by the endothelium in the regulation of the inducible nitric oxide synthase expression in rat isolated aortic vessels. Interleukin-1 beta (0.03 U/L) stimulated nitrite release by the aortic vessels. The nitrite released was less in vessels with endothelium than in deendothelialized aortic segments. This effect was accompanied by a reduced expression of the inducible nitric oxide synthase in the aortic rings with endothelium. Exogenous angiotensin II inhibited IL-1 beta-stimulated inducible nitric oxide synthase protein expression in both deendothelialized vessels and those with endothelium, although with reduced ability on the aortic segments with endothelium by a nitric oxide-independent mechanism. In the aortic rings with endothelium, either inhibition of the AT-1 receptor with losartan or blocking of angiotensin II generation with fosinopril enhanced interleukin-1 beta-stimulated inducible nitric oxide synthase protein expression. In conclusion, the endothelium decreases inducible nitric oxide synthase expression in the vascular wall. Angiotensin II released from endothelial cells is a main mediator responsible for this inhibition through an AT-1-type receptor-dependent mechanism. (Hypertension. 1997;30:1191-1197.)