Central adiposity is a significant determinant of obesity-related hypertension risk, which may arise due to the pathogenic
inflammatory nature of the abdominal fat depot. However, the influence of pro-inflammatory adipokines on blood pressure
in the obese hypertensive phenotype has not been well established in Saudi subjects. As such, our study investigated
whether inflammatory factors may represent useful biomarkers to delineate hypertension risk in a Saudi cohort with and
without hypertension and/or diabetes mellitus type 2 (DMT2). Subjects were subdivided into four groups: healthy lean
controls (age: 47.965.1 yr; BMI: 22.962.1 Kg/m2), non-hypertensive obese (age: 46.165.0 yr; BMI: 33.764.2 Kg/m2),
hypertensive obese (age: 48.666.1 yr; BMI: 36.567.7 Kg/m2) and hypertensive obese with DMT2 (age: 50.866.0 yr; BMI:
35.366.7 Kg/m2). Anthropometric data were collected from all subjects and fasting blood samples were utilized for
biochemical analysis. Serum angiotensin II (ANG II) levels were elevated in hypertensive obese (p,0.05) and hypertensive
obese with DMT2 (p,0.001) compared with normotensive controls. Systolic blood pressure was positively associated with
BMI (p,0.001), glucose (p,0.001), insulin (p,0.05), HOMA-IR (p,0.001), leptin (p,0.01), TNF-a (p,0.001) and ANG II
(p,0.05). Associations between ANG II and TNF-a with systolic blood pressure remained significant after controlling for BMI.
Additionally CRP (p,0.05), leptin (p,0.001) and leptin/adiponectin ratio (p,0.001) were also significantly associated with
the hypertension phenotype. In conclusion our data suggests that circulating pro-inflammatory adipokines, particularly ANG
II and, TNF-a, represent important factors associated with a hypertension phenotype and may directly contribute to
predicting and exacerbating hypertension risk.