Effect of acute saline volume loading on renal sympathetic nerve activity in anaesthetised fructose-fed and fat-fed rats

Abstract

Experiments were conducted to investigate the effects of activation of cardiopulmonary vagal afferent nerve endings by acute saline volume expansion on sympathetic efferent renal nerve activity in anaesthetised fat-fed and fructose-fed Wistar rats. Four weeks of fat feeding caused obesity in the Wistar rats which was associated with a mild elevation in blood pressure (118±4 mmHg vs. 105±1 mmHg in the lean control rats, P<0.05). Fructose feeding in Wistar rats for 4 weeks also elicited an elevation of blood pressure (113±4 mmHg, P<0.05) and plasma glucose levels (6.3±0.3 mmol/l vs. 4.0±0.3 mmol/l lean control rats, P<0.01). The fat-fed rats displayed a higher basal renal sympathetic nerve activity (RSNA) value when compared with the lean rats (3.9±0.4 mV/s vs. 2.8±0.4 mV/s, P<0.05) whereas the RSNA levels were similar in all the other rat groups. The power spectral analysis of RSNA showed the basal values of percentage power at heart rate frequency were significantly higher in Wistars fed ad lib ( P<0.01), rats fed on fructose for 2 or 4 weeks ( P<0.01 and P<0.05, respectively) and fat-fed rats ( P<0.01) when compared to the lean diet-controlled rats. Acute volume expansion (10% body wt) over 40 min caused efferent renal sympatho-inhibition in all the animal groups. The pattern and magnitude of response in MAP, RSNA, and power spectral analysis parameters to the volume expansion were similar in the lean control rats, the Wistar and fructose fed rats but was greater in the fat-fed rats ( P<0.05) as compared to the lean control rat. The profile of the reduction in percentage power at heart rate frequency to volume expansion was greater ( P<0.05) in the fat-fed rat than in the lean control rats. The present data demonstrates that the reflex efferent renal sympatho-inhibition to volume expansion was impaired in the diet-induced obese rat but not in the fructose fed rats. This suggests that a defect in the neuro-humoral regulation of kidney control of extracellular fluid volume is present which may contribute to the mild hypertension in the obese rat.