| Objects:To study the impacts and mechanisms of blood pressure and vessel tone by prenatal hypoxia in spontaneous hypertension rats offspring.Methods:24 pregnant rats were randomly divided into control group?21%oxygen?and hypoxia group?10.5%oxygen?from gestation day 6 to day 21.At day 21,5 pregnant rats received cesarean section in each group.Body weight of fetuses were recorded.Others were allowed to give birth naturally.Neonatal rats were fed normally and raised until12-weeks-old.Healthy male offspring were used for experiments.Body weight were recorded.Systolic blood pressure were recorded weekly;The responses of PE-mediated vasoconstriction in mesenteric arteries in both groups were detected through DMT vascular tension detection system.Specific blockerand antagonistof L-type-Ca2+channel?Cav1.2?were used to test Ca2+-dependent vasoconstriction mechanism.The Ca2+-sensitive vasoconstrictionmechanismwasstudiedbyblockingRhoA/Rock pathway.Acetylcholine?Ach?was applied to detect thevasodilatation.The expression levels of related genes and protein were detected by RT-PCR and Western-blot.Results:Hypoxia group showed obvious lower body weight and higher blood pressure compared to that of control group.The maximal contract to PE and Bay K8644 in mesenteric arteries was stronger in hypoxia group.Also,nifedipine and Y27632 suppressed PE-induced response in both groups,but the extent of inhibition was greater in hypoxia group.In addition,ACh-mediated relaxation was weaker in hypoxia offspring.The expression of mRNA and protein of Cav1.2 and Rock1 were up-regulated by prenatal hypoxia while Rock2 and MYPT1 remaind unchanged.Conclutions:These data suggested that hypoxia in pregnancy altered the systolic blood pressure and PE-mediated vasoconstrictions in mesenteric arteries of SHR male offspring,which could be partially attributed to increased expression of Cav1.2and alteration of RhoA/Rock-mediated pathways. |
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