Figure 8.

Schematic depiction of the possible mechanism of action of 3-hydroxyphenylacetic acid (3-HPAA) involving the production of NO in endothelial cells and activation of sGC in vascular smooth muscle cells (green arrows) and other pathways investigated in the current study. SKCa—small conductance Ca²⁺-activated K⁺ channels; IKCa—intermediate conductance Ca²⁺-activated K⁺ channels; M₃—muscarinic receptor subtype M₃; PLC—phospholipase C; DAG—diacylglycerol; PKC—protein kinase C; IP₃—inositol trisphosphate; IP₃R—inositol trisphosphate receptor; SR—sarco/endoplasmic reticulum; TRP—transient receptor potential channel; Ca/CaM—calcium-calmodulin complex; COX—cyclooxygenase; PGs—prostaglandins; eNOS—endothelial nitric oxide synthase; NO—nitric oxide; MEJ—myoendothelial junction; sGC—soluble guanylate cyclase; GTP—guanosine triphosphate; cGMP—cyclic guanosine monophosphate; PKG—protein kinase G; Cav1.2 (L-type)—L-type calcium channels; EC—endothelial cell; VSMC—vascular smooth muscle cell.