Role of AT2R (Angiotensin Type 2 Receptor) in Maintaining Sodium-Potassium Balance
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
See related article, pp 622–630
Sodium (Na+) balance is flow dependent and occurs along the nephron because of basic communication between nephron segments in response to Na+ levels and to maintain Na+ delivery to the distal convoluted tubule (DCT).1 Decreased distal Na+ delivery increases Na+ reabsorption by facilitating epithelial Na+ channel activity in the distal nephron at the expense of K+ excretion to maintain the ionic gradient. This process is very dynamic and is affected by multiple factors. Ang-II (angiotensin-II) and its AT1R (ang-II type 1 receptor) constitute a well-known antinatriuretic hormone/receptor system that promotes Na+ reabsorption and decreases distal Na+ delivery. Now, there is ample evidence demonstrating the natriuretic role of the AT2R (angiotensin type 2 receptor) in normal and pathological conditions. Along the nephron, the proximal and distal tubules are the primary sites where AT2R is expressed, albeit at a very low receptor density. However, the expression of renal AT2R increases in pathological conditions, such as obesity and diabetes mellitus, including in the diabetic human kidney. AT2R expressed in the proximal tubule seems to play a significant role in natriuresis potentially via inhibition of sodium transporters, such as the NKA (Na+-K+-ATPase). According to at least 1 study, AT2R-mediated natriuresis is not impacted by inhibitors of the distal tubule transporter NCC (Na+-Cl− cotransporter) and epithelial Na+ channel activity.2
Compared with that discussing the role of AT2R in Na+ excretion, literature describing the effect of AT2R on the K+ channel is limited only to neuronal cells3 and the renal outer medullary K+ channel4 in the cortical collecting duct. Wu et …