*4.2. Renal APN in BP Control*

APN is widely distributed in the kidney and has been detected in glomeruli, mesangial cells, and on the luminal surface of tubules [47,58]. Renal APN generates AngIV [59,60], and infusion of AngIV in the renal artery increased sodium excretion [61–63], an effect related to the reduced activity of basolateral tubular Na-K-ATPase [64]. This mechanism may also participate in the adaptative response to increased salt intake, thus protecting against hypertension. Moreover, abnormalities in renal APN have also been observed in several models of experimental hypertension. Thus, the Goldblatt model showed increased APN activity in the renal cortex of the non-clipped kidney [41] and APN protein abundance and activity in the kidney were increased in Dahl salt-resistant versus Dahl salt-sensitive animals (64). APN has also been associated with essential hypertension in humans [65].
