Abstract: The present study was undertaken to quantify the renal salt and water excretory functions in response to acute unilateral renal denervation in Sprague Dawley (SD) and spontaneously hypertensive (SHR) rats in an attempt to characterize the relative contribution of renal sympathetic nerve activity (RSNA) to renal functional excretory responses in normotensive and hypertensive conditions. Adult male SD and SHR rats were fasted overnight, anesthetized with pentobarbitone sodium (60 mg kg-1 i.p.), denervated by application of phenol to the left renal artery and maintained on an intravenous (i.v.) infusion of normal saline for 2 h. Throughout this period, six urine and plasma samples were collected at 20 min intervals to study kidney function parameters. The data showed that there was a significantly higher (p<0.05) amount of sodium and water excretions in the urine of denervated SD and SHR rats as compared to their innervated counterparts. No significant difference in the renal salt and water excretions was seen between innervated SD and SHR rats; however, the difference was significant (p<0.05) following removal of renal sympathetic input. No appreciable changes in the mean arterial blood pressure (MAP) and plasma sodium (PNa) were observed in denervated SD and SHR rats as compared to the innervated ones; yet, MAP values were significantly higher (p<0.05) in denervated and innervated SHR rats in comparison to the denervated and innervated SD rats. Moreover, PNa in denervated SHR rats, which was significantly higher (p<0.05) in SHR rats as compared to SD rats prior to renal denervation, tended to approximate the one in denervated SD rats. In conclusion, this study confirmed the significant role played by the renal nerves in the control of renal functions. Diuresis and natriuresis are typical responses to acute renal denervation (ARD) in SD and SHR rats. Enhanced salt and water excretion following ARD in SHR rats suggests high renal sympathetic nerve discharge in these animals and highlights the significant contribution of renal nerves to the genetic model of essential hypertension.