Hypertension in response to IL-6 during pregnancy: role of AT1-receptor activation
Babbette LaMarca1, Joshua Speed1, Lillian Fournier Ray1, Kathy Cockrell1, Gerd Wallukat2, Ralf Dechend2, Joey Granger1
1Departments of Obstetrics and Gynecology/Physiology, Center for Excellence in Renal and Cardiovascular Research, University of Mississippi Medical Center, Jackson, MS, USA; 2HELIOS Clinic, Charite, Campus-Buch and Max-Delbrueck Center, Berlin, Germany
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.
Keywords: cytokines, pregnancy, hypertension, renin angiotensin system, inflammation
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