Renal sympathetic nerves (RSN)

The renal nerves comprise a complex network of efferent sympathetic and afferent sensory fibers that innervate the kidneys, primarily traveling within the adventitia of the renal arteries. The efferent fibers regulate key physiological processes including the stimulation of renin release from juxtaglomerular cells, the promotion of tubular sodium and water reabsorption, and the modulation of renal vascular resistance [1][3]. Conversely, afferent renal nerves transmit sensory information regarding renal ischemia, stretch, and chemical changes back to the central nervous system, which can trigger a systemic increase in sympathetic outflow [2]. In pathological states such as resistant hypertension and chronic heart failure, the renal nerves often exhibit chronic hyperactivity, driving a vicious cycle of sympathetic overstimulation and fluid retention. While traditionally managed with sympatholytic drugs that inhibit neurotransmitter release or receptor binding, the renal nerves have become a primary target for catheter-based renal denervation (RDN) therapies. These procedures use radiofrequency or ultrasound energy to ablate the nerves, effectively lowering blood pressure and reducing sympathetic drive in patients who do not respond to conventional pharmacological interventions [3][4]. [1] DiBona, G. F. (2000). 'Physiology in health and disease: The functions of the renal nerves'. Rev Physiol Biochem Pharmacol. [2] Schlaich, M. P., et al. (2009). 'Renal denervation as a therapeutic approach'. Hypertension. [3] StatPearls (2023). 'Renal Denervation'. [4] Kandzari, D. E., et al. (2022). 'The SPYRAL HTN-ON MED Trial'. The Lancet.

Other names

Renal nervesRenal plexusRenal afferent and efferent nervesRenal sympathetic nerve fibers

The renal nerves act as a pathway for sympathetic communication between the central nervous system and the kidneys. Therapeutic intervention, primarily through renal denervation (RDN) procedures or sympatholytic drugs, aims to interrupt efferent signaling to reduce renin release and sodium retention, and afferent signaling to decrease global sympathetic vasomotor tone [1][2].