However, we found that 1) cold exposure significantly activates EnNaC in rat MA endothelial cells via elevating plasma aldosterone levels and stimulating its downstream regulator; 2) activated EnNaC contributes to cold exposure–induced vascular dysfunction and hypertension; 3) CIH could be ameliorated by pharmacological inhibition of EnNaC, aldosterone/MR, and Sgk1/Nedd4-2 signaling. This evidence concerns the gene NR3C2 and Hypertension.