Long-term treatment with supraphysiological doses of nandrolone decanoate reduces the sensitivity of Bezold–Jarisch reflex control of heart rate and blood pressure

We investigated the influence of long-term treatment with supraphysiological doses of an anabolic-androgenic steroid on the Bezold–Jarisch reflex (BJR) control of heart rate (HR) and diastolic arterial pressure (DAP), and whether this treatment induced cardiac hypertrophy. Male rats were treated with nandrolone decanoate (ND) (10 mg kg−1 body weight for 8 weeks; DECA) or vehicle (control animals; CON). After 8 weeks of treatment, the BJR was evaluated by bradycardia and hypotension responses that were elicited by serotonin administration (2–32 μg kg−1). Mean arterial pressure (MAP) was assessed and cardiac hypertrophy was determined by the ratio of the left and right ventricle weight/body weight (LVW/BW and RVW/BW, respectively) and by histological analysis. Total body protein (TBP) content was also evaluated. Nandrolone decanoate treatment increased MAP (CON = 99 ± 1 mmHg; DECA = 109 ± 2 mmHg; p < 0.01) but did not change the mean basal HR (CON = 356 ± 13 bpm; DECA = 367 ± 11 bpm). The treatment also induced LV and RV hypertrophy (LVW/BW: CON = 1.86 ± 0.04 mg g−1, DECA = 2.17 ± 0.04 mg g−1, p < 0.01; RVW/BW: CON = 0.42 ± 0.02 mg g−1, DECA = 0.53 ± 0.03 mg g−1, p < 0.05) and reduced the number of myocyte nuclei/high-power field (CON = 23.0 ± 2; DECA = 9.4 ± 1.0; p < 0.01). ND treatment blunted the HR and DAP decreases induced by serotonin. ND determines an increase in the TBP content in DECA group (35 ± 3%; p < 0.01) compared with control animals (18 ± 1%). We conclude that 8 weeks of ND treatment induces anabolic effect, cardiac hypertrophy and an elevation of MAP. This treatment also reduces the sensitivity of the BJR control of bradycardia and blood pressure, possibly due to cardiac hypertrophy. The blunted BJR response could contribute to the MAP elevation in DECA animals.