Neural regulation of the kidney in rats with heart hypertrophy: impact of nitric oxide (NO)

Heart hypertrophy associates with decreased cardiac output and initiates an activation of the sympathetic nervous system. This study investigated whether a volume expansion (VE) mediated inhibition of renal sympathetic nerve activity (RSNA) was impaired in a model of heart hypertrophy and if NO was involved. Groups of male Wistar rats (n=7) were fed a normal diet or given drinking water containing caffeine (61.6 mg/L) plus sc isoprenaline (5 mg/kg every 72 h) for 2 weeks. Following chloralose/urethane anaesthesia, a femoral artery and vein were cannulated to monitor blood pressure (BP) and infuse saline. The left kidney was exposed and the renal nerves placed on recording electrodes. VE comprised a saline infusion at 0.25% bwt/min for 30 min, a 30 min recovery period was allowed, the NO synthase (NOS) inhibitor L‐NAME was given at 10μg/min/kg for 60 min and then a second VE was performed. Data, means ±SEM, were subjected to ANOVA and significance taken at P<0.05. Body weight was lower but heart weight was higher in the hypertrophy group than the normal group, 224±5 versus 233±6g, and 0.96±0.05 versus 0.67±0.02g (both P<0.01). BP, at 96±4 mmHg, rose by 5 and 8% in the normal rats and decreased by 14 and 4% in the hypertrophy group during the 1 st and 2 nd VE (all P<0.05). VE in the normal rats decreased (P<0.001) RSNA by 42% at 30 min but was unchanged in the hypertrophy group. VE with L‐NAME, reduced RSNA by 78% and 33% (both P<0.001) for the normal and hypertrophy rats which were larger (both P<0.001) than those of the 1 st VE. The lack of a VE renal sympatho‐inhibition in heart hypertrophy indicates a deficit in the reflex but the enhanced responses with L‐NAME suggests a potential role of NO in the brain.