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Proinflammation andHypertension: APopulation‐BasedStudy Vanhala MaunoKautiainen HannuKumpusalo Esko2008 год

Proinflammation and Hypertension: A Population‐Based Study
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Аннотация: There is evidence that proinflammation may be linked to the development of hypertension (HT). We examined the association of both the interleukin‐1 beta (IL‐1 β ) and the interleukin 1‐receptor antagonist (IL‐1ra) with future blood pressure (BP) and HT occurrence (BP ≥ 140/90 mmHg, or antihypertensive drug) in a population‐based prospective study. Our study consisted of 396 (147 men and 249 women) middle‐aged, baseline apparently healthy, normotensive subjects participating in a 6.5‐year follow‐up study. Subjects with high‐sensitivity CRP (hs‐CRP) < 10 mg/L were excluded at the initial visit. At follow‐up, the occurrence of HT was 32%. The levels of baseline IL‐1 β and IL‐1ra were significantly higher for subjects who developed HT during the follow‐up than for those who did not (IL‐1 β ; 0.67 ± 0.62 pg/mL versus 0.56 ± 0.32 pg/mL, P = .020 and IL‐1ra; 184 ± 132 pg/mL versus 154 ± 89 pg/mL, P = .007). After adjustments for age, follow‐up time, sex, baseline systolic BP, and BMI, our results confirm a statistically significant ( P = .036) linear association between the quartiles of IL‐1 β and change of systolic BP during the study. After adjustments for age, follow‐up time, sex, and BMI, our results also show a linear association between incident HT and the quartiles of IL‐1ra. ( P = .026). These results provide evidence that proinflammation may precede BP elevation and HT.
Год издания: 2008
Авторы: Vanhala Mauno, Kautiainen Hannu, Kumpusalo Esko
Издательство: Hindawi Publishing Corporation
Источник: Mediators of Inflammation
Ключевые слова: Adipokines, Inflammation, and Metabolic Diseases, Stress Responses and Cortisol, Hormonal Regulation and Hypertension
Другие ссылки: Mediators of Inflammation (PDF)
Mediators of Inflammation (HTML)
DOAJ (DOAJ: Directory of Open Access Journals) (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
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