孕期白细胞介素-6引起的高血压：1型血管紧张素受体激活的作用
Hypertension in response to IL-6 during pregnancy: role of AT1-receptor activation.
作者信息
Lamarca Babbette, Speed Joshua, Ray Lillian Fournier, Cockrell Kathy, Wallukat Gerd, Dechend Ralf, Granger Joey
机构信息
Departments of Obstetrics and Gynecology/Physiology, Center for Excellence in Renal and Cardiovascular Research, University of Mississippi Medical Center, Jackson, MS, USA.
出版信息
Int J Interferon Cytokine Mediat Res. 2011 Nov;2011(3):65-70. doi: 10.2147/IJICMR.S22329.
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.
摘要
背景
白细胞介素6（IL-6）的增加以及血管紧张素II 1型受体激动性自身抗体（AT1-AA）被认为是子痫前期胎盘缺血与高血压之间的重要联系。方法：本研究的目的是确定向正常妊娠（NP）大鼠输注IL-6（5纳克/天）是否会增加平均动脉压（MAP）和AT1-AA。在存在和不存在血管紧张素1型受体（AT1R）拮抗剂氯沙坦的情况下分析MAP。结果：慢性输注IL-6后，MAP从102±2 mmHg增加到118±4 mmHg，AT1-AA从0.7±0.3个变时单位增加到14.1±1.4个变时单位。氯沙坦预处理的大鼠对IL-6的MAP反应消失（NP + L组为85±4 mmHg，IL-6 + L组为85±3 mmHg）。结论：这些数据表明IL-6刺激AT1-AA，并且AT1R的激活介导了孕期IL-6诱导的高血压。
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