APN as a Regulator of Salt Sensitivity

Renal APN regulates mechanisms that facilitate renal sodium excretion after increased saline intake, producing a coordinated decrease in Na-K-ATPase abundance on the basal side of the tubule (by endocytosis) and a reduction in sodium transporters (by internalization) [66–68].

APN abundance is higher in Dahl salt-resistant rats. In these animals, APN may reduce basolateral Na+-K+-ATPase as a protective mechanism in response to the increased saline intake [64]. Reduced tissue and plasma APN levels have also been reported in the L-NAME model but not in the controls [68]. In conclusion, renal tubule levels of APN can regulate sodium excretion and, therefore, salt sensitivity and BP.
