Fig. 9.

Schematic diagram showing the possible signaling pathways through which ER stress mediates enhanced endothelium-derived contractile factor (EDCF) contractions in the aorta of the SHR. We suggest that this enhancement is because 1) ER stress contributes to increased COX-1 expression and prostanoid release by enhancing phosphorylation of ERK 1/2 and cPLA₂ at Ser⁵⁰⁵, contributing to the enhanced EDCF response in the aorta of the SHR, 2) ER stress inhibition prevents reactive oxygen species (ROS)-stimulated enhanced contraction and ROS production, and 3) chemical chaperones TUDCA or PBA lower blood pressure in the SHR. EC, endothelial cell; SMC, smooth muscle cell.