Figure 2.

KCC is implicated in atherosclerosis and is a potential therapeutic target for hypertension. Potassium chloride channel (KCC) in vascular cells is regulated via the platelet-derived growth factor (PDGF) and nitric oxide (NO), both of which are implicated in atherosclerosis and vasodilation respectively. PDGF regulates KCC through the dimerization of PDGF receptors (PDGFR) and the subsequent activation of phosphoinositide 3-kinase (PI3K). Through an unknown mechanism, PI3K activates protein phosphatase 1 (PP1) which dephosphorylates and actives KCC. Activation of KCC could enhance the phenotypic switching of vascular smooth muscle cells (VSMCs) into a diseased state. NO regulates KCC via the nitric oxide/cyclic guanosine monophosphate/protein kinase G (NO/cGMP/PKG) pathway. PKG activates PP1 through an unknown mechanism leading to KCC activation and consequent vasodilation. KCC could be a potential therapeutic target for hypertension. Apelin is cardioprotective and a common modulator of both pathways.