Title:Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation
VOLUME: 18 ISSUE: 28
Author(s):D. Di Raimondo, A. Tuttolomondo, C. Butta, S. Miceli, G. Licata and A. Pinto
Affiliation:U.O.C. Medicina Vascolare, Dipartimento Biomedico di Medicina Interna e Specialistica, Universita degli Studi di Palermo, Piazza delle Cliniche n° 2, 90127 Palermo.
Keywords:Renin-angiotensin-aldosteron system (RAAS), ACE inhibitors, angiotensin recpetor blockers, inflammation, cardiovascular disease, angiotensin II (Ang II), aldosterone, receptor antagonists, fibrinogen, CRP
Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm
that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely
related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every
class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone,
agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid
receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation
and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors,
actually there is no convincing evidence indicating that ACEi’s reduce plasma levels of major inflammatory markers in hypertension
models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to
atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished
using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking
AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies
by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.
