Also, ANG II increases phospholipase D (PLD) activity and DNA and protein synthesis to a greater extent in VSMCs from hypertensive than normotensive subjects, and the ANG II effects are partially inhibited by treating the cells with the PKC inhibitors chelerythrine and calphostin C. These data suggest that the increased oxidative stress and growth-promoting effects of ANG II in VSMCs from hypertensive patients may involve increased activity of PLD- and PKC-dependent pathways and further support a role of these pathways in the vascular remodeling associated with HTN [103]. Here, PRRT2 is linked to hypertensive disorder.