Increased inflammatory biomarkers in hypertensive type 2 diabetic patients: improvement after angiotensin II type 1 receptor blockade

Touyz, Rhian M.; Savoia, Carmine; He, Ying; Endemann, Dierk; Qian, Pu; Ko, Eun A.; DeCiuceis, Carolina; Montezano, Augusto C.; Schiffrin, Ernesto L.

doi:10.1016/j.jash.2007.01.009

Cited by 26 publications

(12 citation statements)

References 50 publications

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“…In hypertension, vascular remodeling has an important Ang II-dependent component as evidenced by clinical investigations demonstrating that angiotensin-converting enzyme (ACE) inhibition or AT 1 receptor blockers prevented or reversed structural and mechanical changes. [42][43][44] In our study, significant vascular alterations were observed in both resistance and conduit arteries. Small mesenteric arteries of Ang II-infused c-Src +/+ mice exhibited increased media thickness, CSA, and vascular stiffness, responses that also present in c-Src +/− mice.…”

Section: Discussionsupporting

confidence: 52%

c-Src Inhibition Improves Cardiovascular Function but not Remodeling or Fibrosis in Angiotensin II–Induced Hypertension

Callera

Antunes

et al. 2016

Hypertension

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Section: Discussionsupporting

confidence: 52%

c-Src Inhibition Improves Cardiovascular Function but not Remodeling or Fibrosis in Angiotensin II–Induced Hypertension

Callera

Antunes

et al. 2016

Hypertension

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“…29 We showed recently that, in high-risk hypertensive patients, BP control obtained mainly with drugs that antagonize components of the renin-angiotensin-aldosterone system, specifically using angiotensin receptor blockers, improves vascular structure 6 and ameliorates systemic inflammation. 29 Aldosterone may in part mediate actions that are usually attributed to the direct effect of angiotensin II, such as vascular remodeling, increased oxidative stress, and inflammation of the vascular wall and the heart. 8,30 Mineralocorticoids and, in particular, aldosterone may activate inflammatory pathways in the cardiovascular system.…”

Section: Discussionmentioning

confidence: 99%

Selective Mineralocorticoid Receptor Blocker Eplerenone Reduces Resistance Artery Stiffness in Hypertensive Patients

Savoia¹,

et al. 2008

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Abstract-Some antihypertensive agents may improve resistance artery remodeling in hypertensive patients whereas other agents may not, for similar blood pressure reduction. We questioned whether the selective mineralocorticoid receptor blocker eplerenone improves resistance artery remodeling in hypertensive patients versus the ␤-blocker atenolol. Sixteen hypertensive patients were randomly assigned to double-blind daily treatment with eplerenone or atenolol. Resistance arteries from gluteal subcutaneous tissue were assessed on a pressurized myograph. After 1 year of treatment, systolic and diastolic blood pressures were similarly well controlled in both groups. Endothelial function did not change with treatment in either group. Media/lumen ratio and cross-sectional area were unchanged in either the atenolol or the eplerenone group. In atenolol-treated patients, the arterial wall became stiffer, whereas in the eplerenone-treated patients, it became less stiff and similar to that of a normotensive control group. The media collagen/elastin ratio was reduced only after eplerenone treatment. Circulating concentrations of osteopontin, monocyte chemoattractant protein-1, basic fibroblast growth factor, interleukin-8, and interleukin-10 were significantly reduced only by eplerenone. However, plasma interleukin-1 receptor a concentration was significantly reduced by both drugs. In conclusion, in hypertensive patients, blood pressure control for 1 year with atenolol was associated with increased wall stiffness of resistance arteries, whereas eplerenone treatment was associated with reduced stiffness, decreased collagen/elastin ratio, and a reduction in circulating inflammatory mediators. These data raise the possibility that eplerenone treatment of hypertensive patients when normalizing blood pressure could potentially be associated with better vascular protection and outcomes than the ␤-blocker atenolol, which remains to be demonstrated. Key Words: aldosterone Ⅲ vascular remodeling Ⅲ extracellular matrix Ⅲ collagen Ⅲ elastin Ⅲ inflammatory biomarkers N ormalization of elevated blood pressure (BP) in hypertensive individuals is associated with reduced targetorgan damage and incident cardiovascular morbidity and mortality. 1 Small artery structural alterations may precede many clinical manifestations of end-organ damage in hypertensive patients 2 and predict the occurrence of future cardiovascular events. 3 Activation of the renin-angiotensinaldosterone system has been associated with increased cardiovascular morbidity and mortality in hypertensive patients. We and others have shown that antihypertensive drugs that interfere with the renin-angiotensin-aldosterone system exert potentially beneficial effects on vascular structure beyond BP control in hypertensive patients at variable risk for cardiovascular disease 4 -7 by improving the functional and anatomic alterations of resistance arteries typically found in experimental and human hypertension and which participate in increased peripheral resistance.Aldosterone is a mine...

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“…Touyz et al (2007) [260] In patients with hypertension and type 2 diabetes IL-6, IL-18, sICAM, and MCP-1 levels were reduced by valsartan (three-fold, P < .05). Only IL-18 was reduced by atenolol compared with pretreatment levels.…”

Section: Valsartan (Vs Atenolol)mentioning

confidence: 96%

“…Touyz et al, tested the hypothesis that in patients with hypertension and type 2 diabetes, hence with a condition of low-grade systemic inflammation, blood pressure (BP) reduction with the ARB valsartan, or with a beta blocker, atenolol, is associated with a decreased inflammatory response [260]. Normotensive subjects and hypertensive patients with type 2 diabetes (40 to 70 years of age) participated in the study.…”

Section: Valsartan (Vs Atenolol)mentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

111

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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.

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Increased inflammatory biomarkers in hypertensive type 2 diabetic patients: improvement after angiotensin II type 1 receptor blockade

Cited by 26 publications

References 50 publications

c-Src Inhibition Improves Cardiovascular Function but not Remodeling or Fibrosis in Angiotensin II–Induced Hypertension

c-Src Inhibition Improves Cardiovascular Function but not Remodeling or Fibrosis in Angiotensin II–Induced Hypertension

Selective Mineralocorticoid Receptor Blocker Eplerenone Reduces Resistance Artery Stiffness in Hypertensive Patients

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

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