It has been demonstrated that the respiratory responses to hypercapnia are enhanced in obese adult humans. In rats, high-fat diet induces dyslipidemia and hyperglycemia and increases body fat. Thus, the aim of the present study was to evaluate the ventilatory responses to hypercapnia, the mean arterial pressure (MAP) and the angiotensin type 1 receptors (AT1r) expression in the nucleus of the tract solitary (NTS) in rats treated with high-fat diet for 6 weeks. Male Hotzman rats (300-320 g) had ad libitum access for 6 weeks to either the standard rat chow diet (CD) that contained 23 g of protein, 49 g of carbohydrates and 4 g of total fat per 100 g of diet or the high-fat diet (HFD) composed of 20 g of protein, 20 g of total fat and 48 g of carbohydrate per 100 g of diet (n = 8-10/group). Changes in ventilation (VE), respiratory frequency (fR), tidal volume (VT), mean arterial pressure (MAP) and heart rate (HR) to chemoreflex activation by hypercapnia (7% CO2) were measured in conscious rats using pletismography method 6 weeks after starting the access to CD or HFD. Values are means ± S.E.M., compared by ANOVA or Student t test. Rats treated with HFD showed increased body mass (422 ± 6, vs. CD: 409 ± 3 g), glycemia (157 ± 6, vs. CD: 133 ± 5 mg/dl), total plasma cholesterol (72.3 ± 3, vs. CD: 64.5 ± 2 mg/dl), plasma triacylglycerol (56.4 ± 4, vs. CD: 38.6 ± 2 mg/dl), baseline MAP (116 ± 2, vs. CD: 106 ± 2 mmHg) and AT1r in the NTS (0.14 ± 0.03, vs. CD: 0.05 ± 0.02) (all p < 0.05), without changes in baseline VE, VT and fR. However, HFD treated rats had increased VE (1250 ± 58, vs. CD: 1021 ± 69 ml/min/kg) and fR (140 ± 7, vs. CD: 122 ± 4 breath/min) without changes in VT (8.9 ± 0.3, vs. 8.3 ± 0.5 ml/kg respectively) during 5 minute exposure to hypercapnia. These results suggest that high-fat diet increases baseline MAP and VE to hypercapnia. Although the mechanisms involved on respiratory changes are not known yet, AT1r overexpression in the NTS may contribute to the hypertension in HFD animals.