Vascular activation of K+ channels and Na+-K+ ATPase activity of estrogen-deficient female rats

The goal of the present study was to evaluate vascular potassium channels and Na+-K+-ATPase activity in estrogen deficient female rats. Female rats that underwent ovariectomy were assigned to receive daily treatment with placebo (OVX) or estrogen replacement (OVX + E2, 1 mg/kg, once a week, i.m.). Aortic rings were used to examine the involvement of K+ channels and Na+-K+-ATPase in vascular reactivity. Acetylcholine (ACh)-induced relaxation was analyzed in the presence of L-NAME (100 μM) and K+ channels blockers: tetraethylammonium (TEA, 5 mM), 4-aminopyridine (4-AP, 5 mM), iberiotoxin (IbTX, 30 nM), apamin (0.5 mM), charybdotoxin (ChTX, 0.1 mM) and iberiotoxin plus apamin. When aortic rings were pre-contracted with KCl (60 mM) or pre-incubated with TEA (5 mM), 4-aminopyridine (4-AP, 5 mM) and iberiotoxin (IbTX, 30 nM) plus apamin (0.5 μM), the ACh-induced relaxation was less effective in the ovariectomized group. Additionally, 4-AP and IbTX decreased the relaxation by sodium nitroprusside in all groups but this reduction was greater in the ovariectomized group. Estrogen deficiency also increased aortic functional Na+-K+ ATPase activity evaluated by K+-induced relaxation. L-NAME or endothelium removal were not able to block the increase in aortic functional Na+-K+ ATPase activity, however, TEA (5 mM) restored this increase to the control level. We also found that estrogen deficiency increased superoxide anion production and reduced nitric oxide release in aortic ring from ovariectomized animals. In summary, our results emphasize that the process underlying ACh-induced relaxation is preserved in ovariectomized animals due to the activation of K+ channels and increased Na+-K+ ATPase activity.