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Aim: Obesity frequently co-exists with hypertension (HTN). Hypothalamus neuropeptides such as neuropeptide Y (NPY) and alpha-melanocyte stimulating hormone (a-MSH) interact with leptin, an anorexic peptide produced mainly by adipose tissue and are involved in the regulation of appetite, energy balance and sympathetic nervous system (SNS) activity, possibly contributing to blood pressure (BP) elevation. We compared plasma NPY and a-MSH levels between patients with or without hypertension and/or obesity and the differences in these neuropeptides between patients with or without pathological heart echo findings, aiming to investigate the possible role of these peptides in obesity induced HTN. Patients and Methods: 160 non-diabetic, treatment-naïve individuals were randomly recruited from our outpatient clinics. Study population was divided into 6 groups, according to body mass index-BMI (OB=obese, OW=overweight, NW=normal weight) and blood pressure. Waist circumference (WC) and heart rate (HR) were also recorded. A heart echo was performed and plasma NPY and a-MSH levels were measured for all participants. Results: Plasma NPY levels and HR were higher in OW and OB hypertensives compared with NW hypertensives. OW and OB hypertensives had also higher NPY concentrations compared with OW and OB normotensives, respectively. However, in NW patients, plasma NPY concentrations did not differ between hypertensives and normotensives. Patients with central obesity (COB) had also higher NPY levels compared with patients without COB, a difference also observed in hypertensives but not in normotensive patients. Furthermore, plasma NPY concentrations were significantly correlated with BMI, WC, HR, systolic and diastolic BP. Patients with left ventricle hypertrophy had higher plasma NPY levels compared with those with normal findings, but this was not seen in hypertensives. The majority of these differences were also observed in male and female patient populations. In contrast, plasma a-MSH levels were similar in all study groups. Conclusions: These results suggest that NPY may be involved in obesity-related HTN, possibly via increased SNS activity. Further investigation is needed to elucidate the role of both NPY and a-MSH in obesity-related HTN.