-
Views
-
Cite
Cite
Vicente Lahera, Victoria Cachofeiro, Natalia de las Heras, Interplay of Hypertension, Inflammation, and Angiotensin II, American Journal of Hypertension, Volume 24, Issue 10, October 2011, Page 1059, https://doi.org/10.1038/ajh.2011.142
Close - Share Icon Share
Extract
Inflammation plays a key role in the pathogenesis of several cardiovascular diseases such as atherosclerosis, heart failure, and hypertension. Many studies have reported that clinical and experimental hypertension is associated with enhanced inflammatory mediators such as C-reactive protein (CRP) and cytokines at both tissue and circulating levels.1 This inflammatory situation could be primarily related with the elevated mechanical forces exerted against the arterial wall. In vitro studies have shown that elevated shear stress and circumferential strain are associated with overexpression of adhesion molecules, cytokines, and transcription factors such as NFκB and AP-1 in the arterial wall.2,3 In addition, circulating and paracrine factors associated with hypertension such as the renin–angiotensin system (RAS) could participate in this systemic inflammatory response. Angiotensin II plays an important role in functional and vascular alterations associated with hypertension through its proliferative, fibrotic, oxidative, and inflammatory actions. The inflammatory effect of angiotensin II is mediated, at least in part, through the activation of NFκB and the subsequent production of inflammatory mediators including interleukin (IL)-6 and IL-1β. We have previously demonstrated that treatment with an AT1 receptor antagonist reduced elevated IL-6 and IL-1β in spontaneously hypertensive rats,4 where this effect was associated with a reduction of NFκB and an enhancement of IκB vascular expressions.
