Hypertension: an autoimmune disease?

Tervaert, Jan Willem Cohen

doi:10.1038/hr.2011.15

Cited by 7 publications

(6 citation statements)

References 21 publications

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“…Hence, a depressed T cell function is a characteristic of an adaptive immune response underlying hypertension. This concept has been proposed before by studies that put immune perturbation forward among which a depressed T cell function was suggested [38],[39]. An imbalance of T-cell subpopulations might be the root to pathological renal damage [11].…”

Section: Discussionmentioning

confidence: 94%

Irreversible Renal Damage after Transient Renin-Angiotensin System Stimulation: Involvement of an AT1-Receptor Mediated Immune Response

et al. 2013

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Transient activation of the renin-angiotensin system (RAS) induces irreversible renal damage causing sustained elevation in blood pressure (BP) in Cyp1a1-Ren2 transgenic rats. In our current study we hypothesized that activation of the AT1-receptor (AT1R) leads to a T-cell response causing irreversible impairment of renal function and hypertension. Cyp1a1-Ren2 rats harbor a construct for activation of the RAS by indole-3-carbinol (I3C). Rats were fed a I3C diet between 4–8 weeks of age to induce hypertension. Next, I3C was withdrawn and rats were followed-up for another 12 weeks. Additional groups received losartan (20 mg/kg/day) or hydralazine (100 mg/kg/day) treatment between 4–8 weeks. Rats were placed for 24h in metabolic cages before determining BP at week 8, 12 and 20. At these ages, subsets of animals were sacrificed and the presence of kidney T-cell subpopulations was investigated by immunohistochemistry and molecular marker analysis. The development of sustained hypertension was completely prevented by losartan, whereas hydralazine only caused a partial decrease in BP. Markers of renal damage: KIM-1 and osteopontin were highly expressed in urine and kidney samples of I3C-treated rats, even until 20 weeks of age. Additionally, renal expression of regulatory-T cells (Tregs) was highly increased in I3C-treated rats, whereas the expression of T-helper 1 (Th1) cells demonstrated a strong decrease. Losartan prevented these effects completely, whereas hydralazine was unable to affect these changes. In young Cyp1a1-Ren2 rats AT1R activation leads to induction of an immune response, causing a shift from Th1-cells to Tregs, contributing to the development of irreversible renal damage and hypertension.

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Section: Discussionmentioning

confidence: 94%

Irreversible Renal Damage after Transient Renin-Angiotensin System Stimulation: Involvement of an AT1-Receptor Mediated Immune Response

et al. 2013

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“…Furthermore, recent studies suggest that T-cells are involved in the pathogenesis of hypertension and, in particular, in hypertension-associated vascular damage. 10,11 The relation between lower T ang and CSVD may specifically imply a role of T ang in CSVD. Still, the nature of this role remains elusive.…”

Section: Discussionmentioning

confidence: 99%

Angiogenic T-Cells and Putative Endothelial Progenitor Cells in Hypertension-Related Cerebral Small Vessel Disease

Rouhl

Mertens

Oostenbrugge

et al. 2012

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Background and Purpose-Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunction, whereas endothelial progenitor cells (EPC) may attenuate endothelial dysfunction. Their vitality is lower in CSVD. A subset of lymphocytes, angiogenic T-cells, is capable to stimulate EPC function. The purpose of our study was to explore the relation between CSVD manifestations, angiogenic T-cells, and EPC in hypertensive patients with CSVD. Methods-We compared 32 essential hypertensive patients with CSVD (white matter lesions, asymptomatic lacunar infarcts, or microbleeds on 1.5-Tesla MRI) to 29 age-matched and sex-matched hypertensive controls. We counted angiogenic T-cells (CD3 ϩ /CD31 ϩ /CD184

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“…Also, additional comorbidities including obesity, stress and physical inactivity may contribute to the development of hypertension. Proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) are associated with higher blood pressure illustrating the reciprocal link between hypertension and inflammation: the former causes vascular damage and thus induces inflammation via oxidative stress whereas the latter appear to increase arterial stiffness and wall pliability [Cohen Tervaert, 2011; McMaster et al 2015].…”

Section: Traditional Risk Factorsmentioning

confidence: 99%

Cardiovascular risk in rheumatoid arthritis: assessment, management and next steps

Zegkos

Kitas

Dimitroulas

2016

Therapeutic Advances in Musculoskeletal

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Rheumatoid arthritis (RA) is associated with increased cardiovascular (CV) morbidity and mortality which cannot be fully explained by traditional CV risk factors; cumulative inflammatory burden and antirheumatic medication-related cardiotoxicity seem to be important contributors. Despite the acknowledgment and appreciation of CV disease burden in RA, optimal management of individuals with RA represents a challenging task which remains suboptimal. To address this need, the European League Against Rheumatism (EULAR) published recommendations suggesting the adaptation of traditional risk scores by using a multiplication factor of 1.5 if two of three specific criteria are fulfilled. Such guidance requires proper coordination of several medical specialties, including general practitioners, rheumatologists, cardiologists, exercise physiologists and psychologists to achieve a desirable result. Tight control of disease activity, management of traditional risk factors and lifestyle modification represent, amongst others, the most important steps in improving CV disease outcomes in RA patients. Rather than enumerating studies and guidelines, this review attempts to critically appraise current literature, highlighting future perspectives of CV risk management in RA.

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Hypertension: an autoimmune disease?

Cited by 7 publications

References 21 publications

Irreversible Renal Damage after Transient Renin-Angiotensin System Stimulation: Involvement of an AT1-Receptor Mediated Immune Response

Irreversible Renal Damage after Transient Renin-Angiotensin System Stimulation: Involvement of an AT1-Receptor Mediated Immune Response

Angiogenic T-Cells and Putative Endothelial Progenitor Cells in Hypertension-Related Cerebral Small Vessel Disease

Cardiovascular risk in rheumatoid arthritis: assessment, management and next steps

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