Natriuresis obtained by intracerebroventricular infusion of hypertonic NaCl in rats with papillary necrosis.

Raising the sodium concentration in the third cerebral ventricle increases renal sodium, potassium and water excretion. The identification and characterization of the factor(s) mediating the centrally evoked natriuresis would be greatly facilitated if the exact intrarenal effector site were known. We have assessed the importance of inner medullary structures for the effects of CNS stimulation by examining its ability to alter renal excretion in rats with papillary necrosis, induced 2 d earlier with 2-bromoethylamine hydrobromide (BEA), 250 mg kg-1 body wt i.v. Male Lewis x DA rats were divided into a BEA-treated group (n = 6) and a control group receiving vehicle alone (n = 6). In contrast to the white papillae normally seen, the papillae of BEA-treated animals were bright red and showed a clear line of demarcation at their base. The rats were anaesthetized i.p. with Inactin (120 mg kg-1 body wt). Artificial cerebrospinal fluid (CSF) was infused (520 nL min-1) via a cannula into the left lateral ventricle. After 45 min CSF containing 1 M NaCl was used. Stimulation of the control rats with hypertonic CSF increased urine flow rate five-fold (5.4 +/- 0.8 to 27.1 +/- 6.1 microL min-1), Na excretion 23-fold (0.4 +/- 0.1 to 7.6 +/- 1.8 mumol min-1) and K excretion fourfold (0.6 +/- 0.18 to 3.8 +/- 0.5 mumol min-1). When the concentration mechanisms were damaged with BEA, the basal excretion rates of water and Na increased. The natriuretic response to ICV stimulation was severely impaired in these rats, but the kaliuretic effect was sustained.(ABSTRACT TRUNCATED AT 250 WORDS)