., Dechend R, LaMarca B. IL-17-mediated oxidative stress is an important stimulator of AT1-AA and hypertension during pregnancy. Am J Physiol Regul Integr Comp Physiol 303: R353-R358, 2012. First published June 20, 2012 doi:10.1152/ajpregu.00051.2012.-Preeclampsia is associated with autoimmune cells TH17, secreting interleukin-17, autoantibodies activating the angiotensin II type I receptor (AT1-AA), and placental oxidative stress (ROS). The objective of our study was to determine whether chronic IL-17 increases blood pressure by stimulating ROS and AT1-AAs during pregnancy. To answer this question four groups of rats were examined: normal pregnant (NP, n ϭ 20), NPϩIL-17 (n ϭ 12), NPϩtempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) (n ϭ 7) (a superoxide dismutase mimetic that scavenges ROS), and NPϩIL-17ϩtempol (n ϭ 11). IL-17 (150 pg/day) was infused into NP rats while tempol was administered via the drinking water ad libitum. On day 19 blood pressure (MAP) was recorded, and plasma, urine, and tissue were collected for isolation of ROS detected by chemilluminescent technique. Urinary isoprostane was measured by ELISA. AT1-AAs were determined via cardiomyocyte assay and expressed as beats per minute. MAP increased from 98 Ϯ 3 mmHg in NP to 123 Ϯ 3 mmHg in IL-17-infused NP rats. Urinary isoprostane increased from 1,029 Ϯ 1 in NP to 3,526 Ϯ 2 pg·mg Ϫ1 ·day Ϫ1 in IL-17-infused rats (P Ͻ 0.05). Placental ROS was 436 Ϯ 4 RLU·ml Ϫ1 ·min Ϫ1 (n ϭ 4) in NP and 702 Ϯ 5 (n ϭ 5) RLU·ml Ϫ1 ·min Ϫ1 in IL-17-treated rats. Importantly, AT1-AA increased from 0.41 Ϯ 0.05 beats/min in NP rats (n ϭ 8) to 18.4 Ϯ 1 beats/min in IL-17 rats (n ϭ 12). Administration of tempol attenuated the hypertension (101 Ϯ 3 mmHg) ROS (459 Ϯ 5 RLU·ml Ϫ1 ·min Ϫ1 ) and blunted AT1-AAs (7.3 Ϯ 0.6 beats/min) in NPϩIL-17ϩtempol-treated rats. Additionally, AT1 receptor blockade inhibited IL-17-induced hypertension and placental oxidative stress. MAP was 105 Ϯ 5 mmHg and ROS was 418 Ϯ 5 RLU·ml
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