Essential Hypertension

Androulakis, Emmanuel; Tousoulis, Dimitris; Papageorgiou, Nikolaos S.; Tsioufis, Costas; Kallikazaros, Ioannis; Stefanadis, Christodoulos

doi:10.1097/crd.0b013e3181b18e03

Cited by 70 publications

(21 citation statements)

References 85 publications

(77 reference statements)

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“…Angiotensin II acts not only as a vasopressor but also as a paracrine and autocrine hormone to promote cell growth, apoptosis, inflammation and tissue damage that ultimately lead to hypertrophy, fibrosis and heart failure (Paul et al 2006; Androulakis et al 2009). Studies have shown that mice with the Th2 phenotype are predisposed to heart disease (Huber&Lodge, 1986; Liao et al 1993; Afanasyeva et al 2001; Liao et al 2005), although their susceptibility to Ang II-induced cardiac damage (or lack of it) is not known.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin II (Ang II), a potent vasopressor, has been implicated in the inflammatory process (Suzuki et al 2003; Androulakis et al 2009). As Th1/Th2 imbalance plays a role in the pathophysiology of cardiovascular remodelling and dysfunction (Okura et al 1998; Shimizu et al 2004; Yu et al 2005; Yu et al 2006) and Balb/c mice are susceptible to heart disease (Huber & Lodge, 1986; Liao et al 1993), we hypothesized that in Ang II-induced hypertension the Th2-dominant Balb/c strain would develop exacerbated cardiac remodelling and impaired cardiac function, whereas the Th1-dominant C57BL/6 strain would be protected.…”

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confidence: 99%

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Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice

Peng

Yang

Carretero

et al. 2011

Experimental Physiology

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Balb/c mice, which are T-helper lymphocyte 2 (Th2) responders, are highly susceptible to infectious and non-infectious heart diseases, whereas C57BL/6 mice (Th1 responders) are not. Angiotensin II (Ang II) is not only a vasopressor but also a pro-inflammatory factor that leads to cardiac hypertrophy, fibrosis and dysfunction. We hypothesized that Ang II exacerbates cardiac damage in Balb/c but not in C57BL/6 mice even though both strains have a similar level of hypertension. Twelve-week-old male C57BL/6J and Balb/c mice received either vehicle or Ang II (1.4mg kg−1 day−1, s.c. via osmotic minipump) for 8 weeks. At baseline, Balb/c mice exhibited the following: (1) a lower heart rate; (2) an enlarged left ventricular chamber; (3) a lower ejection fraction and shortening fraction; and (4) twice the left ventricular collagen deposition of age-matched C57BL/6J mice. Angiotensin II raised systolic blood pressure (to ~150 mmHg) and induced cardiomyocyte hypertrophy in a similar manner in both strains. While C57BL/6J mice developed compensatory concentric hypertrophy and fibrosis in response to Ang II, Balb/c mice demonstrated severe left ventricular chamber dilatation, wall thinning and fibrosis, leading to congestive heart failure as evidenced by dramatically decreased ejection fraction and lung congestion (significant increase in lung weight), which are both characteristic of dilated cardiomyopathy. Our study suggests that the Th phenotype plays an active role in cardiac remodelling and function both in basal conditions and in hypertension. Angiotensin II-induced dilated cardiomyopathy in Balb/c mice is an ideal animalmodel for studying the impact of the adaptive immune system on cardiac remodelling and function and for testing strategies to prevent or treat hypertension-associated heart failure.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice

Peng

Yang

Carretero

et al. 2011

Experimental Physiology

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“…Factors in the pathophysiology of hypertension noted by Page remain important and our knowledge of these individually are growing, for example, genetic, endocrine, and immune factors [5, 34–38]. Of note, greater attention to renal involvement in hypertension has been combined with greater knowledge of the interaction of renal and neural control [39–43].…”

Section: Pathophysiology Of Essential Hypertensionmentioning

confidence: 99%

From Brain to Behavior: Hypertension's Modulation of Cognition and Affect

Jennings

Heim

2012

International Journal of Hypertension

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Accumulating evidence from animal models and human studies of essential hypertension suggest that brain regulation of the vasculature is impacted by the disease. Human neuroimaging findings suggest that the brain may be an early target of the disease. This observation reinforces earlier research suggesting that psychological factors may be one of the many contributory factors to the initiation of the disease. Alternatively or in addition, initial blood pressure increases may impact cognitive and/or affective function. Evidence for an impact of blood pressure on the perception and experience of affect is reviewed vis-a-vis brain imaging findings suggesting that such involvement in hypertensive individuals is likely.

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“…AngII also causes diapedesis (leukocyte extravasation) in inflammatory cells. It also increases the TGF-β signaling which is one of the main factors involved in the pathogenesis of cardiovascular disorders, including hypertension (18). Based on the findings of clinical and laboratory studies, other components of the RAS, including aldosterone and/or mineralocorticoid receptor (MR) can also lead to oxidative stress and vascular inflammation (19); as a consequence, the administration of aldosterone and MR stimulants increase the serum level of IL-6 and IL-12 (20).…”

Section: Introductionmentioning

confidence: 99%

Relationship between IL-17 and ambulatory blood pressure inpolycystic ovary syndrome

Foroozanfard¹,

Soleimani²,

Arbab³

et al. 2016

J Nephropathol

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BackgroundPolycystic ovary syndrome (PCOS) is one of the most common endocrine disorders with an inflammatory basis. It is associated with hyperandrogenism in women and can be also associated with increased activity of the renin-angiotensin system (RAS). Approximately 5% to 10% of women of reproductive age are affected by this disease. This syndrome is the main cause of infertility. Blood pressure may be one of the complications of the syndrome. ObjectivesIn this study, we sought to assess the role of the IL-17 inflammatory cytokine in increasing blood pressure in patients with PCOS. Patients and MethodsIn this cross-sectional study, after obtaining informed consent, we evaluated 85 patients with PCOS. IL-17 serum level was measured after separating the serum via ELISA method. The results obtained for the two groups of patients with high blood pressure and normal blood pressure were compared with each other. ResultsThe daytime blood pressure was abnormal in eight patients, while it was normal in 72 patients. The blood pressure during the day had a direct correlation with the IL-17serum level; as a result, the mean IL-17 serum level in patients with high blood pressure was 77.10 ± 17.94 ρ g/ml while in those with normal blood pressure it was 55.20 ± 13.71 ρ g/ml (P = 0.001). High blood pressure during the night also showed a direct relation with theIL-17 serum level (P = 0.001). In addition, increasing of ambulatory 24-hourblood pressure was significantly related with IL-17 serum level, in such a way that the IL-17 serum level of people with high blood pressure rose by almost 22 ρg/ml during 24 hours (P = 0.001). ConclusionsOur results showed an association between PCO syndrome and inflammatory factors. The IL-17 serum level was directly associated with the increase in blood pressure.

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Essential Hypertension

Cited by 70 publications

References 85 publications

Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice

Angiotensin II-induced dilated cardiomyopathy in Balb/c but not C57BL/6J mice

From Brain to Behavior: Hypertension's Modulation of Cognition and Affect

Relationship between IL-17 and ambulatory blood pressure inpolycystic ovary syndrome

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