Neural regulation of renal tubular sodium reabsorption and renin secretion

The entire mammalian nephron, including the juxtaglomerular apparatus, receives an exclusive noradrenergic innervation. Renal tubular alpha 1 adrenoceptors mediate the alterations in tubular segmental sodium, chloride, and water reabsorption that occur in response to direct or reflex changes in efferent renal sympathetic nerve activity. Specific tubular segments so identified are the proximal convoluted tubule, the loop of Henle (thick ascending limb), and the collecting duct. Alterations in efferent renal sympathetic nerve activity represent an important physiological contribution to the overall role of the kidney in the regulation of external sodium balance in conscious animals during both dietary sodium restriction and acute and chronic increases in total-body sodium. Progressively more intense activation of the renal nerves recruits a series of adrenergically mediated influences on renin secretion that are additive, ranging from subtle (modulation of nonneural mechanisms without directly causing renin secretion) to marked (renal vasoconstriction, antinatriuresis, high renin secretion rates). Juxtaglomerular granular cell beta 1 adrenoceptors mediate renin secretion responses to frequencies of renal nerve stimulation that do not cause renal vasoconstriction; at higher frequencies of renal nerve stimulation where renal vasoconstriction is present, renal vascular alpha 1 adrenoceptors mediate a portion of the renin secretion response.