ENDOGENOUS ANGIOTENSIN-II PRODUCED BY ENDOTHELIUM REGULATES INTERLEUKIN-1-BETA-STIMULATED NITRIC-OXIDE GENERATION IN RAT ISOLATED VESSELS

The endothelium is a source of several factors that regulate vascular functions. Angiotensin II is one of the main active factors released b y the endothelium. The aim of the present work was to analyze the role of angiotensin II released by the endothelium in the regulation of th e inducible nitric oxide synthase expression in rat isolated aortic ve ssels. Interleukin-1 beta (0.03 U/L) stimulated nitrite release by the aortic vessels. The nitrite released was less in vessels with endothe lium than in deendothelialized aortic segments. This effect was accomp anied by a reduced expression of the inducible nitric oxide synthase i n the aortic rings with endothelium. Exogenous angiotensin II inhibite d IL-1 beta-stimulated inducible nitric oxide synthase protein express ion in both deendothelialized vessels and those with endothelium, alth ough with reduced ability on the aortic segments with endothelium by a nitric oxide-independent mechanism. In the aortic rings with endothel ium. either inhibition of the AT-1 receptor with losartan or blocking of angiotensin II generation with fosinopril enhanced interleukin-1 be ta-stimulated inducible nitric oxide synthase protein expression. In c onclusion, the endothelium decreases inducible nitric oxide synthase e xpression in the vascular wall. Angiotensin II released from endotheli al cells is a main mediator responsible for this inhibition through an AT-1-type receptor-dependent mechanism.