The kidney as a sensor

Abstract

To evaluate the effects of afferent renal nerve activity on reflex control of the cardiovascular system and volume balance. In the kidney, receptors sensitive to mechanical and chemical stimuli have been identified. Afferent fibres from the kidney have been shown to travel along renal nerves and dorsal roots, mainly from T9 to L4, and to project to the central nervous system at spinal and supraspinal levels. Most of the brainstem regions involved in cardiovascular control and several regions of the anterior hypothalamus (including vasopressin-secreting neurons) receive inputs from renal afferents. The electrical stimulation of afferent renal nerve fibres can either increase or decrease systemic arterial pressure. The hypertensive response to electrical stimulation of renal afferents is the result of widespread activation of the sympathetic nervous system, leading to an increase in peripheral vascular resistance. Activation of afferent renal nerve fibres by an intrarenal artery infusion of adenosine elicits sustained increases in arterial pressure, heart rate and cardiac output without changing total peripheral resistance, indicating reflex activation of the sympathetic nervous system, predominantly restricted to the heart. An increase in the plasma vasopressin concentration, observed during the electrical stimulation of renal afferents, might help to mediate the hypertensive response to afferent renal nerve stimulation. The existence of neural renorenal reflexes, by which one kidney can influence the functioning of the opposite kidney, is well established. Contralateral renorenal reflexes, which are inhibitory in nature, are tonically active and mainly control the secretion of renin from juxtaglomerular cells and the tubular reabsorption of sodium and water. The evidence suggests that sensory information from the kidney contributes to the overall regulation of cardiovascular homeostasis and volume balance.