Figure 3.

Role of PKC in hypertension. Genetic, dietary and environmental risk factors, lead to vascular, neural and renal dysfunction, and increased release of various mediators from endothelial cells (ROS, ET-1, ANG II), sympathetic neurons (norepinephrine) and the kidney (ANG II). These mediators could stimulate VSM and activate PKC, as well as Ca²⁺, Rho kinase, and MAPK thereby induce vasoconstriction and VSM growth and proliferation. The interaction of PKC with matrix metalloproteinases (MMPs) in the extracellular matrix (ECM) could contribute to vascular remodeling. Activation of the renin-angiotensin system (RAS) and increased ANG II production induce salt and water retention and increase plasma volume. Persistent increases in peripheral vascular resistance and plasma volume lead to hypertension.