In order to investigate whether the renal sympathetic nerves contribute to the compensatory Na reabsorption observed during furosemide-induced volume contraction, furosemide was administered as constant i.v. infusion (7.5 mg/kg/h) in trained, chronically instrumented rats with or without guanethidine-induced peripheral sympathectomy. In addition, the effect of acute instrumentation was evaluated by measuring renal function before and after furosemide infusion in control rats recovering from surgery and halothane anesthesia. Lithium clearance was used as a marker for proximal tubular Na reabsorption, and [3H]inulin and [14C]tetraethylammonium were used as markers for the glomerular filtration rate and the effective renal plasma flow, respectively. Control values in chronically instrumented sympathectomized rats did not differ from values obtained in chronically instrumented control rats. In acutely instrumented control rats the control value for effective renal plasma flow was 20% lower than in both chronically instrumented groups; this was associated with increased arterial blood pressure and increased renal vascular resistance. There were no differences in the diuretic or the natriuretic furosemide response between chronically instrumented control and chronically instrumented sympathectomized rats, whereas the diuretic and natriuretic responses were reduced in acutely instrumented control rats. This was due to an accentuation of the initial fall in glomerular filtration rate during furosemide infusion. In control animals, either acutely or chronically instrumented, fractional Li excretion increased from 30% to 50% during furosemide peak response, after which it returned toward control values. In sympathectomized rats, the fractional Li excretion increased from 36% to 70% during furosemide peak response, after which it decreased to a steady-state value of 56%.(ABSTRACT TRUNCATED AT 250 WORDS)