Fig. 3
From: Ca2+ signaling in vascular smooth muscle and endothelial cells in blood vessel remodeling: a review
Electrical remodeling in hypertensive VSMCs and ECs. A In hypertensive VSMCs, the expression and activity (cluster formation) of Cav1.2 channels are enhanced. In addition, increased expression of AT1R and IP3R and increased formation of the α1AR-TRPV4 complexes can increase VSMC contractility. B Decreased activity of BKCa channels and dissociation of TRPV4 channel reduce STOCs. Kv channel expression also decreases, resulting in depolarization of the membrane potential. C In ECs, dissociation of TRPV4 channel and eNOS reduces NO production. Activation of Piezo1 channels can cause sustained Ca2+ influx from TRPV4 channels due to sustained high shear stress, enhancing endothelial permeability. In addition, Piezo1 channels activate a NF-κB pathway mediated by panexin1/P2Y2 in response to turbulent laminar flow. D In myoendothelial junctions, downregulation or oxidation of AKAP150 reduce TRPV4 channel activity and reduce EDHF and NO production. Kir2.1 channel and gap junction component proteins are also downregulated in hypertensive ECs and VSMCs localized at the myoendothelial junction. AA: arachidonic acid, AT1R: AngII receptor type 1, EDHF: endothelium-derived hyperpolarizing factor, EET: epoxytrienoic acid, PLA2: phospholipase A2, PM: plasma membrane, SR: sarcoplasmic reticulum, STOC: spontaneous transient outward current, α1AR: α1 adrenergic receptor