6 Effect of placental ischaemia on angiotensin II type 1 receptor autoantibodies (AT1AA) in a non human primate model of experimental preeclampsia

Introduction AT1AA have been shown to contribute to the pathogenesis and clinical syndrome of preeclampsia. The pathogenesis of preeclampsia is primarily attributed to poor placentation and subsequent placental hypoxia. A reduced uterine perfusion pressure rat model of preeclampsia has shown that placental ischaemia is a stimulus for AT1AA mediated hypertension. Objectives Assess the effect of placental ischaemia on the concentration of AT1AA in a non-human primate animal model (Papio Hamadryas) of experimental preeclampsia. Methods Experimental preeclampsia was achieved by surgically induced uteroplaental ischaemia (UPI). Plasma and urine samples were taken pre (day 0) and post UPI (7 days, 14 days, 21 days, 28 days, 35 days). Proteinuria was measured by urine protein to creatinine ratio, blood pressure was measured by intra-arterial radio-telemetry and plasma soluble fms like tyrosine kinase receptor 1 (sFLT-1) levels was measured by ELISA. AT1-AA levels were measured using a species-specific ELISA (MyBiosource). SPSS software was used for analysis, data expressed as mean+SEM and significance set at p Results All animals developed clinical signs of experimental preeclampsia as evidenced by the development of proteinuria and hypertension. There was an average rise in awake and asleep blood pressure (SBP/DBP) 9.7/9.2 mmHg ( p  = 0.028; 0.025) and 5.8/6.7 mmHg ( p  = 0.085; 0.026) respectively. Urinary protein significantly increased by 28.04 + 10 mg/mmol, p  = 0.03. sFlt-1 significantly increased 2 weeks post UPI 5919.5 + 1800 pg/ml compared to pre-UPI 1944.2 + 463 pg/ml, p  = 0.05. AT1AA levels were not significantly different pre 147 + 7 u/ml and post UPI 144 + 8 u/ml p  = 0.44. Conclusions AT1-AA are pre-existing prior to the development of placental hypoxia. Surgically induced placental ischaemia does not induce or alter the levels of AT1-AA.