FIGURE 8.

Model for regulation of resistance artery relaxation by RGS2 in endothelium. Vasodilatory agonists such as ACh activate G_q-coupled receptors in endothelial cells of resistance arteries to evoke Ca²⁺ transients that stimulate eNOS for producing NO and K channels (SK_Ca and IK_Ca) for producing endothelium-derived hyperpolarizing factor (EDHF). RGS2 accelerates G protein deactivation by functioning as a GAP for Gα subunits of the G_i or G_q classes. RGS2 deficiency in endothelium is proposed to impair vascular relaxation by augmenting G_i signaling, which inhibits EDHF production by mechanisms yet to be determined. IP₃, inositol 1,4,5-trisphosphate.