The pathway of sympathetic innervation to the kidneys and upper ureter (see Plate 1-15) begins in presynaptic fibers originating in the T10-L1 levels of the IML. These fibers travel through splanchnic nerves to synapse with neurons of the superior mesenteric ganglion, aorticorenal ganglia, and the small ganglia in the periarterial renal plexuses. Postsynaptic fibers reach the kidney and upper ureter via periarterial plexuses and branches.

The pathway of sympathetic innervation to the remainder of the ureters and urinary bladder begins with presynaptic fibers originating in the T12-L2(3) levels of the IML. These fibers travel through lumbar (and possibly sacral) splanchnic nerves and then the intermesenteric (aortic) plexus, then synapse with neurons in the inferior mesenteric ganglion or small ganglia of the aortic/hypogastric plexuses. Postsynaptic fibers descend into the pelvis via aortic, hypogastric, and pelvic (vesical) plexuses to reach the ureters and bladder.

Function. In the kidney, sympathetic tone has numerous effects on both the vasculature and renal tubules. Adrenergic receptors are located throughout the renal cortex and outer stripe of the outer zone of the renal medulla, with the greatest density in the juxtamedullary region of the inner cortex. Graded increases in renal sympathetic tone cause renin release from juxtaglomerular granular cells (see Plate 3-18), increase renal tubular sodium reabsorption, and decrease renal blood flow (by constricting afferent arterioles). These combined effects can contribute to the development and maintenance of hypertension. In experimental animals, for example, renal denervation is known to prevent or ameliorate hypertension. Likewise, in patients with drug-resistant essential hypertension, catheter-based radiofrequency renal denervation results in substantial and sustained reductions in systemic blood pressure.