Neural control of renal tubular sodium reabsorption.
Renal adrenergic nerves are in contact with the basement membranes of tubule cells and, when these nerves are stimulated or ablated, proximal tubular reabsorption of sodium is increased or decreased, respectively. Renal adrenergic nerve activity appears to be regulated by low-pressure cardiopulmonary receptors and high-pressure arterial baroreceptors in response to changes in blood volume. Thus, a decrease in blood volume or in effective circulating blood volume leads to an increase in renal nerve activity, release of norepinephrine, alpha-adrenergic stimulation and increased tubular reabsorption of sodium, whereas an increase in blood volume leads to a decrease in renal nerve activity, a decreased release of norepinephrine, an increased release of dopamine, possible beta-adrenergic stimulation and a decreased tubular reabsorption of sodium.
D000818:Animals; D001485:Basement Membrane / Q000378:metabolism; D001692:Biological Transport; D001810:Blood Volume; D006801:Humans; D007668:Kidney / Q000294:innervation; D007684:Kidney Tubules / Q000378:metabolism*; D009638:Norepinephrine / Q000502:physiology; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D012964:Sodium; D009638:Norepinephrine