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We analysed the sensitivity to β-adrenoceptor agonists in epididymal adipose cells from rats submitted to a stress protocol previously reported to induce alterations in sensitivity to catecholamines in cardiac tissue from rats. Food intake and body weight were lower, whereas adipocytes basal lipolysis was higher (control: 0.59 ± 0.04; stress: 1.00 ± 0.11, μmol glycerol/100 mg total lipids/100 min) in stressed compared to control rats. The responses to isoprenaline (pD2 control: 7.46 ± 0.11; stress: 8.11 ± 0.17), adrenaline (pD2 control: 5.78 ± 0.20; stress: 6.13 ± 0.18), and salbutamol (pD2 control: 5.64 ± 0.28; stress: 5.92 ± 0.34) were sensitized, and the lipolytic responses to norepinephrine (pD2 control: 6.98 ± 0.13; stress: 6.41 ± 0.12) and to BRL37344 (pD2 control: 8.43 ± 0.19; stress: 7.54 ± 0.21) were desensitized. Responses to the higher concentration (100 μm) of isoprenaline (control: 1.80 ± 0.18; stress: 2.24 ± 0.10 μmol glycerol/100 mg total lipids/100 min), epinephrine (control: 1.64 ± 0.17; stress: 2.24 ± 0.14 μmol glycerol/100 mg total lipids/100 min), salbutamol (control: 0.65 ± 0.11; stress: 1.21 ± 0.41 μmol glycerol/100 mg total lipids/100 min), and d-butyryl-cAMP (control: 1.59 ± 0.17; stress: 2.72 ± 0.25) were significantly enhanced in adipocytes from stressed rats. pD2 or maximum response to CGP12177 were not altered. Supersensitivity to isoprenaline was abolished by 50 nm ICI118,551 but was not modified by 100 nm metoprolol. However, subsensitivity to norepinephrine and to BRL37344 was abolished by 100 nm metoprolol. Our results suggest that in epididymal adipocytes from stressed rats there is a desensitization of the response to adrenoceptor agonists mediated by β1-adrenoceptors together with a sensitization of the response mediated by β2-adrenoceptors. β3-adrenoceptors seem to be resistant to the stress effect.—Farias-Silva, E., D. M. Grassi-Kassisse, V. Wolf-Nunes, and R. C. Spadari-Bratfisch. Stress-induced alteration in the lipolytic response to β-adrenoceptor agonists in rat white adipocytes. J. Lipid Res. 1999. 40: 1719–1727.