Neurogenic hypertension: revelations from genome-wide gene expression profiling.
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.
School of Health Sciences, University of Ballarat, Victoria, Australia. f.marques@ballarat.edu.au
Francine Z
FZ
Marques
Brian J
BJ
Morris
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic; D020869:Gene Expression Profiling; D006973:Hypertension / Q000209:etiology / Q000235:genetics*; D051379:Mice; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis*; D022661:RNA, Untranslated / Q000032:analysis / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D017382:Reactive Oxygen Species / Q000378:metabolism
D012333:RNA, Messenger; D022661:RNA, Untranslated; D017382:Reactive Oxygen Species; D009569:Nitric Oxide