Subtitle Adipokines and hypertension Background Epicardial adipose tissue (EAT) shares a common embryological origin with intra-abdominal visceral fat depots and has been shown to be quantitatively related to various components of the metabolic syndrome, including hypertension. However, it is still not certain whether the secretions of adipokines from EAT and other fat depots differ between patients with and without hypertension. Methods Epicardial, mediastinal, and subcutaneous adipose tissues were collected from 36 patients with coronary artery disease underwent elective coronary artery bypass surgery. Levels of adiponectin, resistin, and leptin in adipose tissue-conditioned media were determined by ELISA. Hypertension was defined as patients being treated for hypertension or having a seated systolic blood pressure of ≥140 mm Hg or a diastolic blood pressure of ≥ 90 mm Hg. Results Overall, releases of adiponectin (∼2-fold), resistin (∼20-fold), and leptin (∼2-fold) were significantly higher in EAT than in subcutaneous adipose tissue, whereas only leptin release (∼2-fold) was increased in mediastinal than in subcutaneous adipose tissue. Compared to patients without hypertension (n = 10), hypertensive patients (n = 26) were associated with a significantly increased level of resistin (by 80%, p = 0.031) in subcutaneous adipose tissue-conditioned media. Despite no differences in levels of adipokines in EAT-conditioned media between patients with hypertension and those without, hypertensive patients had a significantly lower EAT/subcutaneous adipose tissue adiponectin ratio (1.9 ± 0.6 vs 3.8 ± 1.5, p = 0.014), after adjustments for age, gender, body-mass index, waist circumference, and conventional risk factors. Conclusions The co-existence of hypertension is associated with changes in adipokine secretions in both EAT and subcutaneous adipose tissue in patients with coronary artery disease. This finding provides a novel pathophysiologic link between hypertension and coronary artery disease.