Cunningham Mark W, West Crystal A, Wen Xuerong, Deng Aihua, Baylis Chris
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi;
Department of Physiology and Functional Genomics, Department of Medicine, University of Florida College of Medicine, Gainesville, Florida; and.
Am J Physiol Regul Integr Comp Physiol. 2015 Jun 1;308(11):R945-56. doi: 10.1152/ajpregu.00141.2014. Epub 2015 Mar 25.
Oxidative stress and inflammation are risk factors for hypertension in pregnancy. Here, we examined the 24-h mean arterial pressure (MAP) via telemetry and the nitric oxide (NO) and redox systems in the kidney cortex, medulla, and aorta of virgin and pregnant rats treated with a high-fat/prooxidant Western diet (HFD), ANG II, and TNF-α. Female Sprague-Dawley rats were given a normal diet (ND) or a HFD for 8 wk before mating. Day 6 of pregnancy and age-matched virgins were implanted with minipumps infusing saline or ANG II (150 ng·kg(-1)·min(-1)) + TNF-α (75 ng/day) for 14 days. Groups consisted of Virgin + ND + Saline (V+ND) (n = 7), Virgin + HFD +ANG II and TNF-α (V+HFD) (n = 7), Pregnant + ND + Saline (P+ND) (n = 6), and Pregnant + HFD + ANG II and TNF-α (P+HFD) (n = 8). After day 6 of minipump implantation, V+HFD rats displayed an increase in MAP on days 7, 8, and 10-15 vs. V+ND rats. P+HFD rats, after day 6 of minipump implantation, showed an increase in MAP only on day 7 vs. P+ND rats. P+HFD rats had a normal fall in 24-h MAP, hematocrit, plasma protein concentration, and osmolality at late pregnancy. No change in kidney cortex, medulla, or aortic oxidative stress in P+HFD rats. P+HFD rats displayed a decrease in nNOSβ abundance, but no change in kidney cortex NOx content vs. P+ND rats. Pregnant rats subjected to a chronic HFD and prooxidant and proinflammatory insults have a blunted increase in 24-h MAP and renal oxidative stress. Our data suggest renal NO bioavailability is not altered in pregnant rats treated with a HFD, ANG II, and TNF-α.
氧化应激和炎症是妊娠期高血压的危险因素。在此，我们通过遥测技术检测了高脂/促氧化剂西式饮食（HFD）、血管紧张素II（ANG II）和肿瘤坏死因子-α（TNF-α）处理的未孕和妊娠大鼠肾皮质、髓质和主动脉中的24小时平均动脉压（MAP）、一氧化氮（NO）和氧化还原系统。雌性Sprague-Dawley大鼠在交配前8周给予正常饮食（ND）或HFD。妊娠第6天和年龄匹配的未孕大鼠植入微量泵，输注生理盐水或ANG II（150 ng·kg-1·min-1）+TNF-α（75 ng/天），持续14天。分组包括未孕+ND+生理盐水（V+ND）（n = 7）、未孕+HFD+ANG II和TNF-α（V+HFD）（n = 7）、妊娠+ND+生理盐水（P+ND）（n = 6）以及妊娠+HFD+ANG II和TNF-α（P+HFD）（n = 8）。在植入微量泵第6天后，与V+ND大鼠相比，V+HFD大鼠在第7、8和10 - 15天MAP升高。在植入微量泵第6天后，与P+ND大鼠相比，P+HFD大鼠仅在第7天MAP升高。P+HFD大鼠在妊娠晚期24小时MAP、血细胞比容、血浆蛋白浓度和渗透压正常下降。P+HFD大鼠肾皮质、髓质或主动脉氧化应激无变化。与P+ND大鼠相比，P+HFD大鼠nNOSβ丰度降低，但肾皮质NOx含量无变化。接受慢性HFD以及促氧化剂和促炎刺激的妊娠大鼠24小时MAP和肾氧化应激的升高减弱。我们的数据表明，用HFD、ANG II和TNF-α处理的妊娠大鼠肾NO生物利用度未改变。
