Centro de Investigación Biomédica y Aplicada (CIBAP), Escuela de Medicina, Facultad de Ciencias Médicas, Universidad de Santiago de Chile (USACH), Santiago 9170020, Chile.
Escuela de Enfermería, Facultad de Ciencias Médicas, Universidad de Santiago de Chile, Santiago 9170020, Chile.
Int J Mol Sci. 2022 Oct 8;23(19):11965. doi: 10.3390/ijms231911965.
A crucial etiological component in fetal programming is early nutrition. Indeed, early undernutrition may cause a chronic increase in blood pressure and cardiovascular diseases, including stroke and heart failure. In this regard, current evidence has sustained several pathological mechanisms involving changes in central and peripheral targets. In the present review, we summarize the neuroendocrine and neuroplastic modifications that underlie maladaptive mechanisms related to chronic hypertension programming after early undernutrition. First, we analyzed the role of glucocorticoids on the mechanism of long-term programming of hypertension. Secondly, we discussed the pathological plastic changes at the paraventricular nucleus of the hypothalamus that contribute to the development of chronic hypertension in animal models of prenatal undernutrition, dissecting the neural network that reciprocally communicates this nucleus with the locus coeruleus. Finally, we propose an integrated and updated view of the main neuroendocrine and central circuital alterations that support the occurrence of chronic increases of blood pressure in prenatally undernourished animals.
胎儿编程中的一个关键病因学组成部分是早期营养。事实上,早期营养不良可能导致血压和心血管疾病(包括中风和心力衰竭)的慢性增加。在这方面,目前的证据支持了几种涉及中枢和外周靶标变化的病理机制。在本综述中,我们总结了神经内分泌和神经可塑性的改变,这些改变是与早期营养不良后慢性高血压编程相关的适应性机制的基础。首先,我们分析了糖皮质激素在高血压长期编程机制中的作用。其次,我们讨论了下丘脑室旁核的病理性塑性变化,这些变化有助于产前营养不良动物模型中慢性高血压的发展,剖析了这个核与蓝斑之间相互交流的神经网络。最后,我们提出了一个综合和更新的观点,即主要的神经内分泌和中枢循环改变支持了在产前营养不良的动物中发生慢性血压升高的情况。