It is worth noting that, either on its own or in combination with deficient gap junction transmission, KCa over-activation may significantly diminish conducted hyperpolarization and/or vasodilation during old age (≥24-month-old mouse skeletal muscle arteries [38], and ≥64-year-old human coronary arteries; [63]), hypertension (Cx40-deficient mice [146]), hyperhomocysteinemia (cystathionine β-synthase mouse gluteus maximus arterioles [147]), and chronic hyperglycemia (diabetic mouse mesenteric arteries [148]). This evidence concerns the gene CSN3 and hypertensive disorder.