The sympathetic nervous system controls kidney excretion: arterial receptors and pressure reflexes

Because the kidneys receive wide sympathetic distribution, changes in sympathetic activity can alter the kidney's sodium and water excretion, as well as regulate extracellular fluid volume under a number of conditions. For example, when blood volume decreases due to haemorrhage, pressure in the pulmonary blood vessels and other low-pressure areas of the chest decreases, causing the sympathetic nervous system activation reflex. This in turn increases renal sympathomimetic activity, has a number of effects that reduce the excretion of sodium and water: (1) constriction of the renal artery, reduces glomerular filtration rate (GFR) if severe sympathetic activation; (2) increased renal tubular water and salt reabsorption; and (3) stimulates renin release and increases Ang II and aldosterone formation, both of which increase tubular reabsorption. If the reduction in blood volume is large enough to relieve systemic arterial pressure, further activation of the sympathetic nervous system occurs due to a decrease in the tension of the artery receptors located in the carotid artery sinus and the aorta. All of these reflexes together play an important role in the rapid recovery of blood volume occurring in acute conditions such as haemorrhage. Additionally, the renal sympathetic inhibition reflex can contribute to the rapid elimination of excess circulatory fluid that occurs after eating a meal containing large amounts of salt and water.