Proinflammation and Hypertension: A Population-Based Study

Vanhala, Mauno; Kautiainen, Hannu; Kumpusalo, Esko

doi:10.1155/2008/619704

Cited by 21 publications

(9 citation statements)

References 25 publications

(35 reference statements)

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“…In our study, we observed a PAR-1-dependent pro-inflammatory state in mice after Ang II infusion measured by increased IL-1β, IL-6, TNF-α, MCP-1, CXCL1 and CXCL2 expression in the aorta. Consistent with this observation, a study showed that increased plasma levels of IL-1β, a cytokine involved in monocyte activation, precedes changes in BP in HTN [50]. Furthermore, IL-6, MCP-1 and especially TNF-α were shown to be essential for the pathologic effects of Ang II on the vasculature by increasing oxidative stress, activating fibroblasts and attracting T cells [47, 51].…”

Section: Discussionmentioning

confidence: 77%

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Antoniak

Cardenas²,

Buczek³

et al. 2016

Cardiology

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Background: Angiotensin II (Ang II) plays an important role in cardiovascular disease. It also leads to the activation of coagulation. The coagulation protease thrombin induces cellular responses by activating protease-activated receptor 1 (PAR-1). We investigated whether PAR-1 contributes to Ang II-induced cardiovascular remodeling and inflammation. Methods and Results: PAR-1^+/+ (wild-type; WT) and PAR-1^-/- mice were infused with Ang II (600 ng/kg/min) for up to 4 weeks. In WT mice, this dose of Ang II did not cause a significant increase in blood pressure but it did cause pathological changes in both the aorta and the heart. Ang II infusion resulted in vascular remodeling of the aorta, demonstrated by a significant increase in medial wall thickening and perivascular fibrosis. Importantly, both parameters were significantly attenuated by PAR-1 deficiency. Furthermore, perivascular fibrosis around coronary vessels was reduced in Ang II-treated PAR-1^-/- mice compared to WT mice. In addition, PAR-1 deficiency significantly attenuated Ang II induction of inflammatory cytokines and profibrotic genes in the aortas compared to WT mice. Finally, PAR-1 deficiency had no effect on Ang II-induced heart hypertrophy. However, the heart function measured by fractional shortening was less impaired in PAR-1^-/- mice than in WT mice. Conclusion: Our data indicate that PAR-1 plays a significant role in cardiovascular remodeling mediated by a blood pressure-independent action of Ang II.

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Section: Discussionmentioning

confidence: 77%

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Antoniak

Cardenas²,

Buczek³

et al. 2016

Cardiology

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“…Expression of endocan increases during inflammation when endothelium is activated by tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1 β) 16). It has been shown that circulating levels of these cytokines are increased in hypertensive patients 18). Endocan is also elevated in HT and is correlated with hsCRP 19).…”

Section: Discussionmentioning

confidence: 99%

Endocan and Non-Dipping Circadian Pattern in Newly Diagnosed Essential Hypertension

et al. 2016

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Background and ObjectivesNon-dipper hypertension is frequently accompanied by endothelial dysfunction and activation. Previous studies suggested that endocan may be a novel endothelial dysfunction marker. This study aims to investigate the association between circadian blood pressure (BP) pattern and plasma endocan levels together with high-sensitivity C-reactive protein (hsCRP) in patients with newly diagnosed untreated hypertension.Subjects and MethodsTwenty-four hour ambulatory blood pressure monitoring was recorded in 35 dipper, 35 non-dipper hypertensives and 35 healthy controls. Endocan levels were measured by enzyme-linked immunosorbent assay. Serum levels of hsCRP were also recorded.ResultsDespite similar daytime and 24-hour average BP values between dippers and non-dippers, statistically significant high nocturnal BP was accompanied by a non-dipping pattern (Systolic BP: 132±9 vs. 147±11 mmHg; Distolic BP: 80±7 vs. 91±9 mmHg, respectively, p<0.001 for both). Non-dipper patients demonstrated higher endocan levels compared to dippers and normotensives (367 (193-844) pg/mL, 254 (182-512) pg/mL and 237 (141-314) pg/ml, respectively, p<0.001). HsCRP levels were significantly higher in non-dippers than the other groups (p=0.013). In a multivariate logistic regression analysis, endocan (p=0.021) and hsCRP (p=0.044) were independently associated with a non-dipping pattern.ConclusionElevated endocan levels were found in non-dipper groups. Endocan and hsCRP were found to be independently associated with a non-dipping pattern. We suggest that elevated levels of endocan in non-dipper hypertensive patients might be associated with a longer duration of exposure to high BP. These results point to the possible future role of endocan in selection of hypertensive patients at higher risk or target organ damage.

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“…146 Blood pressure has been found to be significantly associated with plasma levels of sICAM-1, IL-6, IL-1b, and IL-1-receptor antagonist (IL-1ra) in healthy, normotensive males and females. 9,11,147 These studies show that even in the early stages of hypertension, inflammatory pathways are activated.…”

Section: Immune System and Hypertension/vasdev Et Almentioning

confidence: 91%

Role of the Immune System in Hypertension: Modulation by Dietary Antioxidants

Vasdev¹,

Stuckless²,

Richardson³

2011

Int J Angiol

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Hypertension is a major health problem worldwide. Individuals with hypertension are at an increased risk for stroke, heart disease, and kidney failure. Although the etiology of essential hypertension has a genetic component, lifestyle factors such as diet play an important role. Insulin resistance is a common feature of hypertension in both humans and animal models affecting glucose and lipid metabolism producing excess aldehydes including methylglyoxal. These aldehydes react with proteins to form conjugates called advanced glycation end products (AGEs). This alters protein structure and function and can affect vascular and immune cells leading to their activation and secretion of inflammatory cytokines. AGEs also act via receptors for advanced glycation end products on these cells altering the function of antioxidant and metabolic enzymes, and ion channels. This results in an increase in cytosolic free calcium, decrease in nitric oxide, endothelial dysfunction, oxidative stress, peripheral vascular resistance, and infiltration of vascular and kidney tissue with inflammatory cells leading to hypertension. Supplementation with dietary antioxidants including vitamins C, E, or B 6 , thiols such as cysteine and lipoic acid, have been shown to lower blood pressure and plasma inflammatory cytokines in animal models and humans with essential hypertension. A well-balanced diet rich in antioxidants that includes vegetables, fruits, low fat dairy products, low salt, and includes whole grains, poultry, fish and nuts, lowers blood pressure and vascular inflammation. These antioxidants may achieve their antihypertensive and anti-inflammatory/immunomodulatory effects by reducing AGEs and improving insulin resistance and associated alterations. Dietary supplementation with antioxidants may be a beneficial, inexpensive, front-line alterative treatment modality for hypertension.

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Proinflammation and Hypertension: A Population-Based Study

Cited by 21 publications

References 25 publications

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation

Endocan and Non-Dipping Circadian Pattern in Newly Diagnosed Essential Hypertension

Role of the Immune System in Hypertension: Modulation by Dietary Antioxidants

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