Other Hormones Regulate Sodium Transport, Including Angiotensin II, Antidiuretic Hormone, Endothelin, and Atrial Natriuretic Peptide
In addition to enhancing sodium transport by stimulating aldosterone release, angiotensin II directly enhances sodium reabsorption in the proximal tubule, thick ascending limb of Henle’s loop, and the collecting duct.
These segments contain specific angiotensin II receptors (AT∣ receptors) that, when activated, increase Na4 transport. In the proximal tubule, angiotensin II stimulates Na4 uptake through the apical Na4∕H4 exchanger and the basolateral Na4(HCOf)3 co-transporter and Na4,K4-ATPase. Angiotensin II also increases expression of the apical Na4∕H4 exchanger and the Na4,K4,2CΓ transporter in the thick ascending limb. In the collecting duct, angiotensin II enhances Na4 transport via the ENaC.In some species, antidiuretic hormone (ADH, vasopressin), which is released when an animal is volume depleted, dehydrated, or hypotensive, enhances salt reabsorption from the thick ascending limb and the collecting duct. The increased salt transport partly results from vasopressin-stimulated increases in the apical Na4,K4,2CΓ co-transporter in the thick ascending limb and the ENaC in the collecting duct. Although ADH stimulation of salt reabsorption in the thick ascending limb has the seemingly paradoxical effect of enhancing the dilution of the tubule fluid, this in fact allows maximal salt and water conservation because water reabsorption in the collecting ducts is enhanced (see Chapter 43).
Endothelin is a peptide hormone produced in the kidney in the collecting duct, endothelial cells, and the thick ascending limb of Henle’s loop. Endothelin acts on specific receptors in the collecting duct and thick ascending limb and increases renal NaCl and water excretion by effects on epithelial transport and renal microcirculation, mediated by nitric oxide and prostaglandins. The transport mechanisms that are inhibited include Na4,K4-ATPase and the apical ENaC.
Atrial natriuretic peptide is produced in the cardiac atria and enhances Na4 excretion in the distal tubules and collecting ducts by inhibiting aldosterone release and also by inhibiting vasopressin effects in the collecting ducts.