Van Vliet B N, Montani J-P
Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Newfoundland, Canada.
Int J Obes (Lond). 2008 Dec;32 Suppl 6:S35-47. doi: 10.1038/ijo.2008.205.
The epidemiology of salt-induced hypertension has been explored in detail in animal studies, in some cases involving exposures to excess dietary salt for much of the animal's lifespan. The results of these studies demonstrate the presence of two distinct time courses of the blood pressure response to a high salt intake: an acute (rapid) blood pressure response occurring over days to weeks, and a slow and progressive blood pressure response that develops over extremely long periods of time, amounting to a significant fraction of the lifespan in normal individuals. The acute form of salt sensitivity is well known in humans, having often been demonstrated as a fall in blood pressure during the period of salt restriction. The slow and progressive form of salt sensitivity has been demonstrated directly in rats and chimpanzees and is also evident in analyses of human cross-population data as a salt dependency of age-associated changes of blood pressure. This slow and progressive component of salt-induced hypertension may be attributable, at least in part, to a progressive rise in the acute salt sensitivity of blood pressure during sustained exposure to high salt. However, a progressively irreversible or 'self sustaining' component of salt-induced hypertension has also been demonstrated in rat studies. This irreversible component has not been completely characterized, but its presence raises the possibility that blood pressure responses to salt restriction may not fully reveal the contribution of salt to blood pressure or the epidemiology of hypertension. These various components of salt sensitivity (acute vs slow, reversible vs irreversible) should be considered in any comprehensive explanation of the effects of salt on blood pressure and especially in experimental studies of the genetic and physiological mechanisms underlying salt-induced hypertension.
在动物研究中已详细探讨了盐诱导性高血压的流行病学,在某些情况下,研究涉及让动物在其大部分生命周期内摄入过量的膳食盐。这些研究结果表明,血压对高盐摄入的反应存在两种不同的时间进程:一种是在数天至数周内出现的急性(快速)血压反应,另一种是在极长时间段内发展的缓慢且渐进性的血压反应,在正常个体中这一反应占生命周期的很大一部分。盐敏感性的急性形式在人类中是众所周知的,通常表现为在限盐期间血压下降。盐敏感性的缓慢且渐进性形式已在大鼠和黑猩猩中得到直接证实,在对人类跨群体数据的分析中也很明显,表现为血压的年龄相关变化对盐的依赖性。盐诱导性高血压的这种缓慢且渐进性成分可能至少部分归因于在持续高盐暴露期间血压急性盐敏感性的逐渐升高。然而,在大鼠研究中也已证实盐诱导性高血压存在一种逐渐不可逆或“自我维持”的成分。这种不可逆成分尚未完全明确其特征,但它的存在增加了这样一种可能性,即对限盐的血压反应可能无法完全揭示盐对血压的影响或高血压的流行病学情况。在对盐对血压影响的任何全面解释中,尤其是在对盐诱导性高血压潜在的遗传和生理机制的实验研究中,都应考虑盐敏感性的这些不同成分(急性与缓慢、可逆与不可逆)。