Proinflammation and Hypertension: A Population-Based Study

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-1β) and the interleukin 1-receptor antagonist (IL-1ra) with future blood pressure (BP) and HT occurrence (BP≥140/90 mmHg, or antihypertensive d...

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Main Authors: Mauno Vanhala, Kautiainen Hannu, Kumpusalo Esko
Format: Article
Language:English
Published: Hindawi Limited 2008-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2008/619704
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spelling doaj-3466b51d47be4b298a5e17ef7120d4a22020-11-24T21:43:42ZengHindawi LimitedMediators of Inflammation0962-93511466-18612008-01-01200810.1155/2008/619704619704Proinflammation and Hypertension: A Population-Based StudyMauno Vanhala0Kautiainen Hannu1Kumpusalo Esko2Unit of Family Practice, Central Hospital of Middle Finland, 40620 Jyväskylä, FinlandDepartment of Rheumatology, Rheumatism Foundation Hospital, 18120 Heinola, FinlandDepartment of Family Medicine, School of Public Health and Clinical Nutrition, Unit of Family Practice, Kuopio University Hospital, Kuopio University, 70211 Kuopio, FinlandThere is evidence that proinflammation may be linked to the development of hypertension (HT). We examined the association of both the interleukin-1 beta (IL-1β) 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-1β and IL-1ra were significantly higher for subjects who developed HT during the follow-up than for those who did not (IL-1β; 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-1β 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.http://dx.doi.org/10.1155/2008/619704
collection DOAJ
language English
format Article
sources DOAJ
author Mauno Vanhala
Kautiainen Hannu
Kumpusalo Esko
spellingShingle Mauno Vanhala
Kautiainen Hannu
Kumpusalo Esko
Proinflammation and Hypertension: A Population-Based Study
Mediators of Inflammation
author_facet Mauno Vanhala
Kautiainen Hannu
Kumpusalo Esko
author_sort Mauno Vanhala
title Proinflammation and Hypertension: A Population-Based Study
title_short Proinflammation and Hypertension: A Population-Based Study
title_full Proinflammation and Hypertension: A Population-Based Study
title_fullStr Proinflammation and Hypertension: A Population-Based Study
title_full_unstemmed Proinflammation and Hypertension: A Population-Based Study
title_sort proinflammation and hypertension: a population-based study
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2008-01-01
description 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-1β) 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-1β and IL-1ra were significantly higher for subjects who developed HT during the follow-up than for those who did not (IL-1β; 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-1β 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.
url http://dx.doi.org/10.1155/2008/619704
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AT kautiainenhannu proinflammationandhypertensionapopulationbasedstudy
AT kumpusaloesko proinflammationandhypertensionapopulationbasedstudy
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