This work was supported by CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico); CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior); FAPDF (Fundação de Amparo a Pesquisa do Distrito Federal) and UCB

(Universidade Católica de Brasília). “
“In the above article, errors were occurred in the Fig. 1A for NPY mRNA CeA panel during manuscript preparation and some images were identical. The correct CeA NPY mRNA panel for Fig. 1A is printed below. The authors regret this error. “
“Dyslipidemia is well recognized as one of the most pernicious metabolic disorders, consisting in an important risk factor of cardiovascular disease, the most prevalent worldwide [5] and [11]. Studies have shown a potential role for antihypertensive drugs on lipid regulation [15]. β-Adrenergic blockers and antagonists MK-2206 mouse of the renin-angiotensin system (RAS) are among the drugs that present better results in the control of metabolic syndrome and dyslipidemia [4], [15], [25], [27] and [29]. Recent studies point out for a role of ACE2/Angiotensin-(1–7)/Mas SCH772984 in vivo axis as an important counterregulatory arm of the RAS, opposing several angiotensin (Ang) II actions in obesity [17], [20] and [21]. Transgenic animals that present a life time increase in plasma Ang-(1–7) showed an improved lipid

and glucose metabolism indicating an important metabolic effect for Ang-(1–7) [20]. On the other hand, mice that lack the Ang-(1–7) receptor, Mas [21], present a metabolic-like syndrome [21]. β-Blockers were also shown to present direct action on metabolic tissues such as muscle, liver and adipose tissue [10], [18] and [26], inhibiting hormone-sensitive lipase

activity in the early weeks of treatment and modulating cholesterol biosynthesis and/or catabolism [26]. In this context, the aim of the present study was to evaluate the effect of the association of a β-blocker, atenolol, and an oral formulation of Ang-(1–7) [12] on lipid metabolism in spontaneously hypertensive rats (SHR). Experiments were performed in male SHR (20 ± 2 weeks old) obtained from the animal facilities Biological Science Institute (CEBIO, UFMG, Belo Horizonte, MG, Brazil) kept in 12 h light/dark cycle room. Vildagliptin Four group of animals received orogastric gavage (1 mL/kg, daily) for 14 weeks of: (a) Ang-(1–7)/hydroxypropyl-β-cyclodextrin [CD-Ang-(1–7), 30 μg/kg/day of the peptide; n = 8]; (b) β-blocker (atenolol, 3 mg/kg/day; n = 8); (c) the association of CD-Ang-(1–7) and atenolol (n = 9) at same doses; and (d) vehicle, hydroxypropyl-β-cyclodextrin (CD, 50 μg/kg/day; n = 9). The proportion of Ang-(1–7) and hydroxypropyl-β-cyclodextrin in the oral formulation was 43% and 57%, respectively. Blood pressure was measured in a group of animals by telemetry for 8 weeks, as previously described [3]. After 14 weeks of treatment, total serum cholesterol and triglycerides were measured by enzymatic method (Kit KATAL Biotecnológica Ind. Com. Ltd., Brazil) in fasted animals.