Effect of renal denervation on phosphate excretion in endotoxemic rats

Our previous studies showed that endotoxin (Et) administration causes hypophosphaturia in the presence of PTH. In this study, we tested the hypothesis that enhanced renal nerve activity during endotoxemia is responsible for hypophosphaturia. Two weeks after bilateral renal denervation, phosphate excretion was examined in endotoxemic Wistar rats (300 g body weight). Renal clearance studies were performed before and after 4 mg/kg body weight Escherichia coli Et administration. Et administration resulted in a marked fall in glomerular filtration rates of innervated rats (n=12, from 2.09 +/- 0.11 ml/min to 0.89 +/- 0.15 ml/min, P<0.005) compared to saline-treated innervated rats (n=7, from 1.98 +/- 0.19 ml/min to 1.76 +/- 0.16 ml/min). The glomerular filtration rate of renal denervated rats was the same for saline-treated rats (n=9, from 2.67 +/- 0.92 ml/min to 1.69 +/- 0.12 ml/min) and Et-treated rats (n=10, from 2.37 +/- 0.19 ml/min to 1.52 +/- 0.07 ml/min). Fractional phosphate excretion was significantly reduced after Et challenge in innervated rats (from 24.0 +/- 3.3% to 11.8 +/- 2.2%, P<0.0001) compared to saline injection in innervated rats (from 26.9 +/- 3.9% to 33.0 +/- 1.6%). Although renal denervation improved the hypophosphaturia in comparison to the innervated rats, fractional phosphate excretion was still lower in Et-treated rats (from 28.8 +/- 5.0% to 18.0 +/- 4.7%, P<0.005) than in saline-treated rats (from 30.2 +/- 6.1% to 38.7 +/- 4.2%). In conclusion, our data did not support the hypothesis that renal nerves have an important role in reducing renal phosphate excretion during acute endotoxemia.