Role of renal nerves in mediating the blunted natriuretic response to acute saline load in obese dogs.

We previously reported that the natriuretic response to an acute sodium load is markedly attenuated in obese dogs. Since obesity is associated with enhanced sympathetic nervous activity, the purpose of this study was to test the hypothesis that obese animals have a reduced ability to excrete a sodium load as a result of abnormal renal nerve function. To test this hypothesis, we determined the effects of an acute sodium load (100 mEq NaCl given as isotonic saline over 60 min) in lean (19.8 +/- 1.0 kg) and obese (25.8 +/- 1.1 kg) dogs. Two surgically designed hemibladders with indwelling catheters were used to collect urine from innervated (INN) and denervated (DNX) kidneys of the same dog. Arterial pressure averaged 99 +/- 3 mm Hg in the obese dogs and 90 +/- 3 mm Hg in the lean dogs. In response to the saline loading in lean dogs, sodium excretion (U(Na)V) increased from 31.0 +/- 7.8 to 145.6 +/- 25.9 microEq/min in the INN kidneys and from 43.1 +/- 10.6 to 151.1 +/- 28.4 microEq/min in the DNX kidneys. In contrast, U(Na)V in obese dogs increased from 10.3 +/- 3.0 to 110.1 +/- 25.5 microEq/min in the INN kidneys and from 24.4 +/- 2.7 to 106.1 +/- 20.6 microEq/min in the DNX kidneys. Cumulative sodium excretory response to sodium loading was significantly lower in the obese dogs. In addition, there was no difference in the cumulative U(Na)V response between the INN (8.4 +/- 2.2 mEq) and DNX kidneys (9.1 +/- 2.3 mEq) of obese dogs. These data indicate that the natriuretic response to an acute saline loading is markedly attenuated in obese dogs. Furthermore, factors other than renal nerves play a role in this abnormal response.