The kidney is innervated with efferent sympathetic nerve fibers reaching the renal vasculature, the tubules, the juxtaglomerular granular cells and the renal pelvic wall. Increases in efferent renal sympathetic nerve activity (ERSNA) reduce renal blood flow and urinary sodium excretion and increase renin secretion rate. In response to normal physiological stimulation, changes in ERSNA contribute importantly to homeostatic regulation of sodium and water balance. The renal sensory nerve fibers are mainly found in the renal pelvic wall. The renal mechanosensory nerves are activated by stretches of the renal pelvic tissue that may occur during increased urine flow rate. Activation of the sensory nerves elicits an inhibitory renorenal reflex response consisting of decreases in ERSNA leading to natriuresis. Increasing ERSNA increases afferent renal nerve activity (ARNA) which in turn decreases ERSNA by activation of the renorenal reflexes. Thus, the afferent renal nerves buffer changes in ERSNA in the overall goal of maintaining sodium balance. In pathological conditions of sodium retention, impairment of the inhibitory renorenal reflexes contributes to the inappropriately increased ERSNA in the presence of sodium retention. Mechanisms involved include increased endogenous angiotensin activity and increased activation of renal pelvic α2-adrenoceptors. In states of renal disease or injury, there is a shift from inhibitory to excitatory reflexes originating in the kidney. Studies in essential hypertensive patients have shown that renal denervation results in long-term reduction in arterial pressure, suggesting an important role for the efferent and afferent renal nerves in hypertension. The mechanisms involved are currently not known. Whether the renal sensory nerves reinnervate the kidney following acute renal denervation will be discussed.