Renal denervation eliminates the natriuretic effect of isotensive sodium loading in conscious rats

Abstract

It was hypothesized that the renal nerve activity (RNA) mediates the natriuretic response to an infusion of NaCl, which does not change mean arterial blood pressure (MABP). This was tested in trained rats supplied with appropriate chronic instrumentation. NaCl solution (1 M) was infused i.v. at 0.02 ml/min/kg (4–5 μl/min) for 2 h during measurements of circulatory, endocrine, and renal variables including RNA. During NaCl infusion RNA decreased by 15% (p<0.05) within 30 min of infusion and reached a nadir of −25% (p<0.05). Renal denervation per se decreased MABP by 15.5 mmHg (p<0.01). In sham operated rats, NaCl infusion increased plasma Na+ by 1.6 mmol/l (repeated measures ANOVA, p<0.03) but left MABP unchanged while heart rate (HR) decreased (455±7 to 427±7 bpm, p<0.0001). Urine flow tended to increase (p=0.056); sodium excretion increased 4‐fold (1.4±0.2 to 6.0±0.6 μmol/min, p<0.0001) while potassium excretion remained stable (2.2±0.3 to 2.3±0.4 μmol/min). NaCl infusion to renally denervated rats decreased HR similarly (423±17 to 393±20 bpm, p<0.005). In contrast, however, sodium excretion remained constant (2.2±0.8 to 3.9±0.9, p=0.68) despite a significant increase in MABP (102±3 to 109±3 mmHg, p<0.0001). It is concluded that a physiological sodium load increases sodium excretion by mechanisms dependent on renal nerves.Supported by the Danish Medical Research Council and the Novo Nordisk Foundation.