Cardiovascular diseases (CVDs) are the most common cause of death from noncommunicable diseases worldwide. In addition to the classical CVD risk factors related to lifestyle and/or genetic background, exposure to an adverse intrauterine environment compromises fetal development leading to low birth weight and increasing offspring susceptibility to develop CVDs later in life, particularly hypertension - a process known as fetal programming of hypertension (FPH). In FPH animal models, permanent alterations have been detected in gene expression, in the structure and function of heart and blood vessels, compromising cardiovascular physiology and favoring hypertension development. This review focuses on the role of the sympathetic nervous system and its interplay with G-protein-coupled receptors, emphasizing strategies that envisage the prevention and/or treatment of FPH through interventions in early life.

中文翻译：

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对高血压胎儿编程中交感神经系统和GPCR相互作用的见解：架起新药理学策略的桥梁。

心血管疾病（CVD）是全世界非传染性疾病最常见的死亡原因。除了与生活方式和/或遗传背景有关的经典CVD危险因素外，暴露于不利的子宫内环境还会损害胎儿发育，导致低出生体重和增加后代在以后生活中发展CVD的易感性，尤其是高血压-这一过程被称为胎儿高血压编程（FPH）。在FPH动物模型中，已经检测到基因表达，心脏和血管的结构与功能的永久性改变，损害了心血管生理，有利于高血压的发展。这篇综述着重于交感神经系统的作用及其与G蛋白偶联受体的相互作用，