Department of Surgery, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Department of Physiology & Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Int J Mol Sci. 2021 Oct 19;22(20):11261. doi: 10.3390/ijms222011261.
In this review, we first provide a brief overview of the nitric oxide synthase (NOS) isoforms and biochemistry. This is followed by describing what is known about NOS-mediated blood pressure control during normal pregnancy. Circulating nitric oxide (NO) bioavailability has been assessed by measuring its metabolites, nitrite (NO) and/or nitrate (NO), and shown to rise throughout normal pregnancy in humans and rats and decline postpartum. In contrast, placental malperfusion/ischemia leads to systemic reductions in NO bioavailability leading to maternal endothelial and vascular dysfunction with subsequent development of hypertension in PE. We end this article by describing emergent risk factors for placental malperfusion and ischemic disease and discussing strategies to target the NOS system therapeutically to increase NO bioavailability in preeclamptic patients. Throughout this discussion, we highlight the critical importance that experimental animal studies have played in our current understanding of NOS biology in normal pregnancy and their use in finding novel ways to preserve this signaling pathway to prevent the development, treat symptoms, or reduce the severity of PE.
在这篇综述中，我们首先简要概述了一氧化氮合酶（NOS）同工型和生物化学。接下来，我们描述了在正常妊娠期间 NOS 介导的血压控制的已知情况。通过测量其代谢物亚硝酸盐（NO）和/或硝酸盐（NO）来评估循环一氧化氮（NO）的生物利用度，在人类和大鼠的正常妊娠期间，NO 的生物利用度一直呈上升趋势，而在产后则下降。相比之下，胎盘灌注不良/缺血会导致全身 NO 生物利用度降低，导致母体内皮和血管功能障碍，随后在子痫前期中发展为高血压。本文最后描述了胎盘灌注不良和缺血性疾病的新出现的危险因素，并讨论了通过靶向 NOS 系统来增加子痫前期患者的 NO 生物利用度的治疗策略。在整个讨论中，我们强调了实验动物研究在我们目前对正常妊娠中 NOS 生物学的理解以及它们在寻找新方法来保护这种信号通路以预防疾病发展、治疗症状或减轻子痫前期严重程度方面的重要性。
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