Reduction of C-reactive protein and the use of anti-hypertensives

Abstract

Inflammatory processes are increasingly recognized as important participants in the pathophysiology of hypertension and cardiovascular disease. Angiotensin II may be to a large degree responsible for triggering vascular inflammation by inducing oxidative stress, resulting in up-regulation of inflammatory mediators. Inflammatory markers such as C-reactive protein are increased in the blood of patients with hypertension and predict the development of cardiovascular disease. Moreover, C-reactive protein may be a pro-inflammatory molecule under certain circumstances. C-reactive protein and high blood pressure in combination have additional predictive value for cardiovascular outcomes, as they contribute as independent determinants of cardiovascular risk. Therapeutic intervention aimed to reduce vascular inflammation in hypertensive patients has been proposed. Recent lines of evidence suggest that lifestyle modification and pharmacological approaches may reduce blood pressure and inflammation in patients with hypertension. Antagonism of the renin-angiotensin system with the selective angiotensin receptor blockers may improve cardiovascular outcome beyond blood pressure control, by reducing vascular inflammation and remodeling.

Figure 1

Scheme of angiotensin II-induced inflammation and vascular damage. Abbreviations: Ang II, angiotensin II; EC, endothelial cell; ECM, extracellular matrix; ET-1, endothelin-1; ICAM, intercellular adhesion molecule; NAD(P)H oxidase, nicotinamide adenine dinucleotide phosphate oxidase; NO, nitric oxide; NF-κB, nuclear factor kappa B; ROS, reactive oxygen species; VCAM, vascular cell adhesion molecule; (-), inhibition or reduction.

Figure 2

Scheme of C-reactive protein-induced inflammation. Abbreviations: Ang II, angiotensin II; AT₁R, angiotensin type 1 receptor; BP, blood pressure; CRP, C-reactive protein; ET-1, endothelin-1; ICAM, intercellular adhesion molecule; NAD(P)H oxidase, nicotinamide adenine dinucleotide phosphate oxidase; NO, nitric oxide; PAI-1, plasminogen activator inhibitor-1; ROS, reactive oxygen species; TPA, tissue plasminogen activator; VCAM, vascular cell adhesion molecule; vWF, von Willebrand factor; (-), reduction.