1. ¹Department of Preventive Medicine and Biometrics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
2. ²Department of Population Health Sciences, University of Wisconsin, Madison, WI, USA
3. ³Centro de Investigación Epidemiológica, Universidad Industrial de Santander, Bucaramanga, Colombia
4. ⁴Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

Correspondence: Dr LE Bautista, University of Wisconsin Medical School, Population Health Sciences, 610 Walnut Street, 703 WARF, Madison, WI 53726-2397, USA. E-mail: lebautista@wisc.edu

Received 16 April 2004; Revised 1 August 2004; Accepted 1 August 2004; Published online 9 September 2004.

Abstract

High blood pressure (HBP) has been associated with elevated C-reactive protein (CRP), a marker of chronic mild inflammation. However, the association between HBP and other inflammatory markers, particularly interleukin 6 (IL-6) and tumour necrosis alpha (TNF-), has not been evaluated in well-controlled studies. We examined the cross-sectional relationship between IL-6, TNF-, and CRP and HBP in a random sample of 196 healthy subjects. All markers were measured in duplicate with high-sensitivity ELISA tests. Three blood pressure (BP) measurments were averaged for the analysis, and subjects with systolic BP 140 and/or diastolic BP 90 mmHg were considered hypertensive. Log binomial regression was used to estimate multivariate-adjusted prevalence ratios (PR) of HBP. Of the subjects, 40% (79) were hypertensive (mean age: 44 years; range 30–64). After adjustment for age, sex, body mass index, family history of HBP, and the level of the other inflammatory markers, subjects in the second (PR: 3.10, P=0.003), third (PR: 2.32; P=0.031), and fourth quartiles (PR: 2.30; P=0.036) of IL-6 were more than twice as likely to be hypertensive than those in the first quartile. Corresponding PR estimates for TNF- levels were 1.41 (P=0.014) for the second; 1.59 (P=0.001) for the third; and 1.61 (P=0.025) for the fourth quartile. The CRP–HBP association was not statistically significant. Our results suggest that TNF- and IL-6 could be independent risk factors for HBP in apparently healthy subjects. Nevertheless, the temporal relationship between elevated inflammation markers and HBP should be ascertained in prospective cohort studies.