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Problem: Preeclampsia (PE), new-onset hypertension during pregnancy accompanied by organ dysfunction, is associated with chronic inflammation including elevated IL- 17, CD4+ T cells, B cells and natural killer (NK) cells. IL-17 can serve as a signal for either the adaptive or innate immune activation.We have previously shown that IL-17 contributes to increased blood pressure in association with elevated TH17 cells, NK cells and B cells secreting angiotensin II type 1 receptor agonistic autoantibodies (AT1- AA) during pregnancy. Moreover, we have shown an important role for CD4+T cells and AT1-AA in multiorgan dysfunction as measured by mitochondrial oxidative stress (mt ROS).However, we do not know the role of adaptive immune cells such as T cells or B cells secreting AT1-AA in mediating the PE phenotype in response to elevated IL-17. Method of study: In order to answer this question, we infused IL-17 (150 pg/day i.p.) into either SpragueDawley (SD) or athymic nude rats via mini-osmotic pump from gestational day (GD) 14--19 of pregnancy. On GD 19, blood pressure was determined and NK cells,mtROS and respiration and AT1-AA production from B cells were measured. Results: Infusion of IL-17 increased blood pressure in the presence or absence of T cells. Mean arterial pressure (MAP) increased with IL-17 from 98 ±2mmHg (n = 12) to 114 ± 2 (n = 12) in SD rats and from 99 ± 4 mmHg (n = 7) versus 115 ± 2 mmHg (n = 7) in athymic nude rats. Similar trends were seen in NK cells and placental mt ROS. Knowing that IL-17 stimulates AT1-AA in SD pregnant rats, we included a group of SD and athymic nude pregnant rats infused with IL-17 and the AT1-AA inhibitor peptide ('n7AAc'). The inhibitor attenuated blood pressure (104.9 ± 3.2, p = .0001) and normalized NK cells andmt function in SD pregnant rats. Importantly, the AT1-AA was not produced in pregnant nude IL-17 treated rats, nor did 'n7AAc' effect MAP, in nude athymic rats. Conclusion: These findings suggest two conclusions; one is that IL-17 causes hypertension and multiorgan dysfunction in the absence of T cells and AT1-AA, possibly through its activation of innate cells and secondly, in the presence of T cells, blockade of the AT1-AA attenuates the effect of IL-17. This study indicates the critical effects of elevated IL-17 during pregnancy and suggest treatment modalities to consider for PE women. [ABSTRACT FROM AUTHOR]

Developing clinically-focused evidence and experience-based approaches to improve maternity care is a national priority. Safety and quality collaborative initiatives related to management of hypertensive disorders of pregnancy are vital in the implementation of improved care. We reviewed the obstetric literature to construct a concise summary of the core pathophysiologic issues, practice principles and clinical interventions which are foundational for physicians providing immediate postpartum care for patients with severe pregnancy-related hypertension (including those with eclampsia, HELLP syndrome, and superimposed preeclampsia inclusive of those with gestational hypertension that develop severe range blood pressures). While based largely upon the American College of Obstetrics and Gynecology (ACOG) Hypertension Task Force Guidelines released in 2013 as well as updated 2018 guidelines set forth by ACOG for hypertensive disorders of pregnancy, this summary goes beyond the basic safety bundles for hypertension management and lays a pathophysiologic foundation for the immediate postpartum care of patients with severe hypertensive disorders of pregnancy. [ABSTRACT FROM AUTHOR]