[PP.35.05] RENAL DENERVATION ATTENUATES CARDIOVASCULAR INFLAMMATION AND REMODELING IN ANGIOTENSIN II-INDUCED HYPERTENSIVE RATS

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Abstract

Objective:

Chronic infusion of angiotensin II (AngII) in experimental animals contributes to hypertension. However, it is uncertain whether the sympathetic nervous system (SNS) plays an important role in this form of hypertension. In this study, we hypothesized that renal denervation (RDN) inhibits angiotensin II (Ang II)-induced cardiovascular inflammation and remodeling.

Design and method:

Male Sprague-Dawley rats weighing between 300 and 350 g were divided into four groups: SHAM group; RDN group; Ang II group; Ang II + RDN group. Blood pressure was measured invasively by telemetry and non-invasively by tail cuff method. Cardiac hypertrophy and function were evaluated by echocardiography. Hearts and aortas were obtained at 14 days to perform western blotting and immunohistochemistry.

Results:

Efficacy of RDN was confirmed by reduction of renal tyrosine hydroxylase expression and norepinephrine levels at two weeks after the procedure. RDN ameliorated the blood pressure elevation and the mesenteric vascular dysfunction induced by Ang II. Ang II caused vascular and cardiac hypertrophy was significantly blunted by RDN compared with sham-operated group, as shown by histopathology and transthoracic echocardiography, respectively. Ang II induction of vascular and myocardial fibrosis and inflammation was suppressed by RDN with concurrent decrease in fibronectin and collagen deposition, macrophage infiltration and MCP-1 expression. Transforming growth factor-β (TGF-β)/Smad signaling pathway and extracellular signal-regulated kinases (ERK) 1/2 were both inhibited by RDN especially in hearts. Most importantly, RDN reduced Ang II-induced aldosterone expression in systemic and local tissues, while tissue levels of norepinephrine were similar among the four groups.

Conclusions:

These results demonstrate that renal denervation attenuates cardiovascular inflammation and remodeling in Ang II-induced hypertensive models, which is likely mediated by both the systemic and local renin-angiotensin system.

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