Introduction: It has been previously recognised that central obesity, as expressed anthropometrically by an increased waist circumference, may contribute to the development of arterial hypertension (HT), in close association with an insulin-resistant state. Endothelin (ET) system activation and an early proinflammatory state have also been suggested to be involved in the association among HT, central adiposity and an increased cardiovascular risk. AIM of this work was to investigate, in subjects with light-to-moderate HT, on the relationship of central obesity to blood pressure (BP) variability and some markers of endothelial activation and/or dysfunction and of systemic inflammation. Methods: Twenty-two male, non-smoker, light-to-moderate HT patients with waist circumference greater than 102 cm (W+) underwent the following measurement: 24 hours pressure BP monitoring (ABPM), body mass index (BMI), fasting blood glucose and insulin with derived HOMA index, lipids, uric acid, C-reactive protein (CRP), V-CAM-1, I-CAM-1, p-selectin, endothelin-1 (ET-1) and microalbuminuria. Data were compared to those of other 22 male patients comparable for age and clinic BP, but with waist circumference less than 102 cm (W-). Results: In W+ group, BMI (p BP was essentially the same along the 24H as well as at both day-and night-time, but in W+ group the variability of 24H systolic BP, as expressed by the standard deviation from its mean value, was significantly higher than in W-(19.6 ± 4.7 mmHg vs 15.0 ± 2.4, panalysis, waist circumference showed positive relationships to: variability of 24H systolic BP (p systolic BP (p<0.005).
Conclusion:The present data show that, in light-to-moderate HT subjects with no evidence of systemic inflammation, a cluster of abnormalities, including higher systolic BP variability, insulin resistance and activation of ET system, is related to the degree of central adiposity. This indicates that even in such patients, without overt obesity or diabetes, central adiposity implicates early alterations potentially leading to an increased cardiovascular risk.