BLUNTED NATRIURETIC RESPONSE TO A HIGH-SODIUM MEAL IN OBESE DOGS - ROLE OF RENAL NERVES

Although the relation between body weight and arterial pressure is wel l established, the mechanisms involved in the pathogenesis of obesity- related hypertension are unclear. However, recent studies suggest that abnormalities in renal function may be involved. The purpose of this study was to test the hypothesis that obese animals have a reduced abi lity to excrete a sodium load as a result of abnormal renal nerve func tion. To quantify the role of renal nerves, we examined changes in ren al hemodynamics and sodium excretion in response to a high-sodium meal (200 mmol Na) in separate innervated and denervated kidneys simultane ously within the same conscious dog. Two surgically designed hemibladd ers with indwelling catheters were used to collect urine from innervat ed and denervated kidneys of the same dog. Body weight averaged 19.9 /- 1.0 kg in the control lean dogs and 25.1 +/- 1.1 kg in the obese do gs. Arterial pressure averaged 101 +/- 4 mm Hg in the obese dogs and 9 0 +/- 4 mm Hg in the lean dogs. In response to the high-sodium meal in lean dogs, urinary sodium excretion increased from 20.8 +/- 4.2 to 18 9.7 +/- 21.2 mu mol/min in the innervated kidneys and from 25.3 +/- 5. 9 to 194.8 +/- 26.9 mu mol/min in the denervated kidneys. In contrast, urinary sodium excretion in obese dogs increased from 9.6 +/- 1.4 to 129.9 +/- 34.3 mu mol/min in the innervated kidneys and from 18.4 +/- 3.7 to 125.2 +/- 30.5 mu mol/min in the denervated kidneys. Cumulative sodium excretion over 140 minutes was significantly lower in the obes e dogs (innervated, 8.4 +/- 2.8 mmol; denervated, 9.8 +/- 2.7 mmol) th an in the lean dogs (innervated, 19.1 +/- 3.3 mmol; denervated, 21.2 /- 4.2 mmol) in response to the high-sodium meal. These data indicate that the natriuretic response to a high-sodium meal is markedly attenu ated in obese dogs. Furthermore, the renal nerves do not appear to pla y a major role in mediating this abnormal response.