School of Health Sciences, University of Ballarat, Victoria, Australia.
Curr Hypertens Rep. 2012 Dec;14(6):485-91. doi: 10.1007/s11906-012-0282-7.
There is now good evidence for a role of the sympathetic nervous system in the etiology of essential hypertension in humans. Although genetic variation is expected to underlie the elevated sympathetic outflow in this complex polygenic condition, only limited information has emerged from classic molecular genetic studies. Recently, progress has been made in understanding neurogenic aspects by determination of global alterations in gene expression in key brain regions of animal models of neurogenic hypertension. Such genome-wide expression studies in the hypothalamus and brainstem support roles for factors such as neuronal nitric oxide synthase, inflammation and reactive oxygen species. A role for non-coding RNAs such as microRNAs, and epigenetic alterations await exploration. Ongoing novel approaches should provide a better understanding of the processes responsible for the increased sympathetic outflow in animal models, as well as essential hypertension in humans. Such information may lead to better therapies for neurogenic hypertension in humans.
现在有充分的证据表明，交感神经系统在人类原发性高血压的发病机制中起作用。虽然遗传变异预计是这种复杂多基因疾病中交感神经传出增加的基础，但经典的分子遗传学研究仅提供了有限的信息。最近，通过确定神经原性高血压动物模型关键脑区的基因表达的整体变化，在理解神经源性方面取得了进展。下丘脑和脑干的全基因组表达研究支持神经元型一氧化氮合酶、炎症和活性氧等因素的作用。非编码 RNA （如 microRNA ）和表观遗传改变的作用仍有待探索。正在进行的新方法应该能够更好地理解导致动物模型中交感神经传出增加以及人类原发性高血压的过程。这些信息可能会为人类神经原性高血压的治疗提供更好的方法。
