Background: Previous studies have shown that a rise in blood pressure (BP) causes chronic inflammation of the endothelium which, in turn, may be responsible for further damage of endothelium and worsening of BP control. On the other hand, several metabolic abnormalities such as dyslipidemia, hyperinsulinemia/insulin-resistance, diabetes, and obesity causes inflammation followed by a later rise in arterial BP. We investigated the role of chronic inflammation in the modulation of BP independently of other traditional cardiovascular risk factors and atherosclerotic lesions. Methods: A total of 537 aged subjects, selected from the whole population of the INCHIANTI cohort, were enrolled. All subjects underwent plasma insulin, glucose, interleukin-6 (IL-6), interleukin- 10 (IL-10), interleukin-1β (IL-1β), interleukin-1 receptor antagonist (IL-1ra), C-reactive protein, and tumor necrosis factor-α (TNF-α levels determination. The IL-6-174 C/G promoter polymorphism was also evaluated. Results: After adjusting for age, sex, insulin resistance syndrome score, and severity of carotid atherosclerosis, serum IL-1β (P <.001), IL-1ra (P <.005) concentration and the insulin resistance syndrome score (P <.001) were the only predictors of diastolic BP. Indeed, age (P <.001), insulin resistance syndrome score (P = .05), IL-1β (P <.05), and severity of carotid atherosclerosis (P <.05) were the only significant predictor of systolic BP. Conclusion: These results suggest that chronic inflammation may play a role in the modulation of arterial BP.
- Blood pressure
- IL-6 genotype
- IL-6, IL-1β
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine