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Previous studies have demonstrated the role of renal kallikrein (rKal), vasoactive kinins and nitric oxide (NO) in regulating the renal response to acute oral protein load (renal reserve, RR). The aim of this study was to evaluate the effects of protein load on renal hemodynamics of obese hypertensive patients and the possible participation of rKal and NO in this response. We studied 14 obese hypertensive patients, (BMI: 32.9 ± 1.1, age: 50.5 ± 0.9 yrs, SBP: 153.5 ± 2.8 mmHg, DBP:96.2 ± 2.2 mmHg, 5 males and 9 females). Hemodynamic and metabolic evaluations were conducted at basal condition and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of plasmatic and urinary NO by the Griess reaction modified, and the urinary excretion of rKal by chromogenic substrate. The mean RR of the patients was 8.0 ± 1.1. After protein load there was a significant increase of urinary kal (0.12 ± 0.04 vs 0.29 ± 0.06 Kal/Cr, p = 0.002), plasma NO (22.1 ± 0.8 vs 25.8 ± 2.1 µM, p = 0.04), RPF (374.2 ± 25.5 vs 438.8 ± 27.2 ml/min, p = 0.02) and GFR (143.7 ± 7.8 vs 151.7 ± 7.0 ml/min, p = 0.0009), but no difference was observed in the urinary concentration of NO. We concluded that in obese hypertensive individuals, the vasodilator capacity of renal vasculature after protein load is preserved and may be mediated by renal kallikrein and NO.