Perinatal Hypoxia In Pregnancy Affected Vascular Contractility Of Uterine Arteries In The Rat

Objectives: This study was to determine the influence of perinatal hypoxia exposure on angiotensin II(Ang II)-mediated vasoconstriction and explore the underlying mechanism.Methods and Results: The treatment of pregnant rats with 10.5% oxygen throughout gestation day 4 to 21(control 21% oxygen) changed uterine arteries, resulting in Ang II-mediated vasocontractility decreased. Measurement of [Ca2+]i in uterine arteries using fluorescent fura-2, the Ca2+ indicator. Ang II-induced arterial diameter changes were grater in control group than those in hypoxia one, while Ang II-induced increased in [Ca2+]i were not obvious differences between control and hypoxia group. Ang II receptor type 1(AT1R), not Ang II receptor type 2(AT2R), causing Ang II-mediated uterine artery vasoconstriction. In addition, Protein kinase C(PKC) antagonist GF109203 X and ROCK antagonist suppressed Ang II-mediated vasoconstriction were lower in the hypoxia group than that of the control. There was an decrease in MYPT-1 and CPI-17 protein expression in hypoxia uterine arteries. Moreover, 20-kDa myosin light chain phosphorylation(MLC20-P) levels were decreased.Conclusions: The results demonstrate that gestational hypoxia exposure on the vascular changes of the uterine arteries, result in Ang II-mediated uterine artery contractility decreased, the calcium sensitization pathways may be responsible for mediating the uterine artery vasoconstriction induced by Ang II.