Puschett J B, Agunanne E, Uddin M N
Department of Medicine, Texas A&M Health Science Center, Temple, TX 76508, USA.
Biochim Biophys Acta. 2010 Dec;1802(12):1246-53. doi: 10.1016/j.bbadis.2010.02.005. Epub 2010 Feb 16.
The bufodienolides are cardiac glycosides which have the ability to inhibit the enzyme, Na(+)/K(+) ATPase (sodium potassium adenosine triphosphatase). They are cardiac inotropes, cause vasoconstriction (and, potentially, hypertension) and are natriuretic. Evidence has accrued over time which supports the view that they are mechanistically involved in volume expansion-mediated hypertension. In this communication, the authors summarize data which support the view that the bufodienolides and, in particular, marinobufagenin (MBG) are involved in the pathogenesis of preeclampsia. In a rat model of the syndrome, MBG causes hypertension, proteinuria, intrauterine growth restriction and increased weight gain. All of these phenotypic characteristics are prevented by an antagonist to MBG, resibufogenin (RBG). The "preeclamptic" animals also develop a vascular leak syndrome, resulting in hemoconcentration. Abnormalities in the MAPK (mitogen-activated protein kinase) system play a role in the mechanism by which MBG produces the abnormalities in the pregnant rat. Studies to discover the relevance of these findings to human preeclampsia are currently underway in several laboratories and clinics.
蟾毒配基是一类强心苷，能够抑制钠钾ATP酶（Na⁺/K⁺ATPase）。它们是强心剂，可引起血管收缩（并可能导致高血压），且具有利钠作用。随着时间的推移，已有证据支持它们在容量扩张介导的高血压发病机制中起作用的观点。在本通讯中，作者总结了支持蟾毒配基，尤其是海蟾蜍精（MBG）参与子痫前期发病机制这一观点的数据。在该综合征的大鼠模型中，MBG会导致高血压、蛋白尿、子宫内生长受限和体重增加。所有这些表型特征都可被MBG拮抗剂脂蟾毒配基（RBG）所预防。“子痫前期”动物还会出现血管渗漏综合征，导致血液浓缩。丝裂原活化蛋白激酶（MAPK）系统异常在MBG导致孕鼠出现异常的机制中起作用。目前，几个实验室和诊所正在开展研究，以探寻这些发现与人类子痫前期的相关性。
