As previously indicated, the upregulatory shift in AT1 receptor expression in the renal cortex leads to higher stimulation of Na-K-ATPase and Na/H exchanger 3 in proximal segments leading to sodium retention and subsequent hypertension [52], as well as increased mechanical stretch-induced glomerular injury culminating in the development of glomerulosclerosis and proteinuria [27]. This evidence concerns the gene SLC9A3 and glomerulosclerosis.