This could be explained by the finding that cerebral but not peripheral B1R are involved in the maintenance of high blood pressure as documented in glucose-fed rats, spontaneously hypertensive rats and angiotensin II-induced hypertension using peptide and non-peptide B1R antagonists (Lungu et al., 2007; De Brito Gariépy et al., 2010). The gene discussed is AGT; the disease is Hypertension.