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

Savoia C, Schiffrin EL - Vasc Health Risk Manag (2007)

Bottom Line: Angiotensin II may be to a large degree responsible for triggering vascular inflammation by inducing oxidative stress, resulting in up-regulation of inflammatory mediators.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.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.

View Article: PubMed Central - PubMed

Affiliation: Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada.

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.

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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.
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fig2: 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.

Mentions: CRP may be more than an inflammatory biomarker of increased cardiovascular risk, as deposits of CRP have been demonstrated by immunohistochemical staining in atherosclerotic plaques (Figure 2), where it co-localizes with the terminal complement complex and appears to be involved in foam cell formation (Torzewski et al 2000). CRP promotes monocyte chemotaxis (Zwaka 2001) and facilitates low-density lipoprotein uptake by macrophages in vitro (Zwaka et al 2001). In endothelial cells, CRP facilitated the release of PAI-1 (Devaraj et al 2003) and endothelin-1 (Verma et al 2002), and increased the expression of cell adhesion molecules (Pasceri et al 2000), reduced NO bioavailability (Venugopal et al 2002), and NO-mediated dilation in the vasculature. In particular, CRP inhibited endothelium-dependent NO-mediated dilatation of coronary arterioles by inducing the generation of superoxide by NAD(P)H oxidase via p38 kinase activation (Qamirani et al 2005). On the other hand, it has been reported that CRP per se does not activate endothelial cells. The latter has been attributed to contamination of CRP preparations with azide and lipopolysaccharide, which could be responsible for the cell activation (Taylor et al 2005). In VSMCs, CRP increased angiotensin type 1 receptor number and ROS formation (Wang et al 2003), as well as activation of the stress-activated protein kinases p38 and c-jun N-terminal kinase (JNK) (Hattori et al 2003). It was recently reported that CRP caused a sustained increase in systolic BP in mice, related to an augmented pressor response to angiotensin II that is associated with a NO-sensitive downregulation of vascular angiotensin type 2 receptor expression (Vongpatanasin et al 2007).


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

Savoia C, Schiffrin EL - Vasc Health Risk Manag (2007)

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.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2350124&req=5

fig2: 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.
Mentions: CRP may be more than an inflammatory biomarker of increased cardiovascular risk, as deposits of CRP have been demonstrated by immunohistochemical staining in atherosclerotic plaques (Figure 2), where it co-localizes with the terminal complement complex and appears to be involved in foam cell formation (Torzewski et al 2000). CRP promotes monocyte chemotaxis (Zwaka 2001) and facilitates low-density lipoprotein uptake by macrophages in vitro (Zwaka et al 2001). In endothelial cells, CRP facilitated the release of PAI-1 (Devaraj et al 2003) and endothelin-1 (Verma et al 2002), and increased the expression of cell adhesion molecules (Pasceri et al 2000), reduced NO bioavailability (Venugopal et al 2002), and NO-mediated dilation in the vasculature. In particular, CRP inhibited endothelium-dependent NO-mediated dilatation of coronary arterioles by inducing the generation of superoxide by NAD(P)H oxidase via p38 kinase activation (Qamirani et al 2005). On the other hand, it has been reported that CRP per se does not activate endothelial cells. The latter has been attributed to contamination of CRP preparations with azide and lipopolysaccharide, which could be responsible for the cell activation (Taylor et al 2005). In VSMCs, CRP increased angiotensin type 1 receptor number and ROS formation (Wang et al 2003), as well as activation of the stress-activated protein kinases p38 and c-jun N-terminal kinase (JNK) (Hattori et al 2003). It was recently reported that CRP caused a sustained increase in systolic BP in mice, related to an augmented pressor response to angiotensin II that is associated with a NO-sensitive downregulation of vascular angiotensin type 2 receptor expression (Vongpatanasin et al 2007).

Bottom Line: Angiotensin II may be to a large degree responsible for triggering vascular inflammation by inducing oxidative stress, resulting in up-regulation of inflammatory mediators.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.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.

View Article: PubMed Central - PubMed

Affiliation: Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal, QC, Canada.

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.

Show MeSH
Related in: MedlinePlus