Intracerebroventricular (i.c.v.) injection of kappa opioid agonists produces diuresis, antinatriuresis and a concurrent increase in renal sympathetic nerve activity (RSNA). The present study examined whether endogenous central kappa opioid systems contribute to the renal excretory responses produced by the stress of an acute hypotonic saline volume expansion (HSVE). Cardiovascular, renal excretory and RSNA responses were measured during control, acute HSVE (5% BW, 0.45 M saline over 30-min) and recovery (70-min) in conscious rats pretreated i.c.v. with vehicle or the kappa opioid receptor antagonist, nor-binaltorphimine (nor-BNI). In vehicle pretreated rats, HSVE produced a marked increase in urine flow rate, but only a low magnitude and delayed natriuresis. RSNA was not significantly suppressed during the HSVE or recovery periods. In nor-BNI-treated rats, HSVE produced a pattern of diuresis similar to that observed in vehicle-treated rats. However, during the HSVE and recovery periods RSNA was significantly decreased and urinary sodium excretion increased in nor-BNI treated animals. In other studies performed in chronic bilateral renal denervated rats, HSVE produced similar diuretic and blunted natriuretic responses in animals pretreated i.c.v. with vehicle or nor-BNI. Thus, removal of the renal nerves prevented nor-BNI from enhancing urinary sodium excretion during HSVE. These findings indicate that in conscious rats, endogenous central kappa opioid systems are activated during hypotonic saline volume expansion to maximize urinary sodium retention by a renal sympathoexcitatory pathway that requires intact renal nerves.