Hypertension in response to IL-6 during pregnancy: role of AT1-receptor activation.

Babbette Lamarca, Joshua Speed, Lillian Fournier Ray, Kathy Cockrell, Gerd Wallukat, Ralf Dechend, Joey Granger
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引用次数: 65

Abstract

BACKGROUND: Increases in interleukin 6 (IL-6) and agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA) are proposed to be important links between placental ischemia and hypertension in preeclampsia. METHODS: The purpose of this study was to determine whether IL-6 (5 ng/day), infused into normal pregnant (NP) rats, increased mean arterial pressure (MAP) and AT1-AA. MAP was analyzed in the presence and absence of an angiotensin type 1 receptor (AT1R) antagonist, losartan, L. RESULTS: MAP and AT1-AA increased from 102 ± 2 to 118 ± 4 mmHg and 0.7 ± 0.3 NP to 14.1 ± 1.4 chronotropic units with chronic IL-6 infusion. MAP responses to IL-6 were abolished in losartan pretreated rats (85 ± 4 in NP + L vs 85 ± 3 mmHg in IL-6 + L). CONCLUSION: These data indicate that IL-6 stimulates AT1-AA and that activation of the AT1R mediates IL-6 induced hypertension during pregnancy.

妊娠期高血压对IL-6的反应:at1受体激活的作用。
背景:白细胞介素6 (IL-6)和血管紧张素II型1受体(AT1-AA)的激动性自身抗体的升高被认为是子痫前期胎盘缺血和高血压之间的重要联系。方法:本研究的目的是观察IL-6 (5 ng/d)输注于正常妊娠大鼠(NP)后是否升高平均动脉压(MAP)和AT1-AA。在血管紧张素1型受体(AT1R)拮抗剂氯沙坦存在和不存在的情况下分析MAP。结果:慢性IL-6输注时,MAP和AT1-AA从102±2增加到118±4 mmHg, 0.7±0.3 NP增加到14.1±1.4变时单位。氯沙坦预处理大鼠对IL-6的MAP反应被消除(NP + L组85±4 mmHg vs IL-6 + L组85±3 mmHg)。结论:这些数据表明IL-6刺激AT1-AA, AT1R的激活介导IL-6诱导的妊娠期高血压。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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