Stanhewicz Anna E, Kenney W Larry
A.E. Stanhewicz and W.L. Kenney are with the Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, USA.
Nutr Rev. 2015 Sep;73 Suppl 2:73-82. doi: 10.1093/nutrit/nuv033.
Physiological regulation of sodium and water intake and output is required for the maintenance of homeostasis. The behavioral and neuroendocrine mechanisms that govern fluid and salt balance are highly interdependent, with acute and chronic alterations in renal output tightly balanced by appropriate changes in thirst and, to a lesser extent in humans, sodium appetite. In healthy individuals, these tightly coupled mechanisms maintain extracellular fluid volume and body tonicity within a narrow homeostatic range by initiating ingestive behaviors and the release of hormones necessary to conserve water and sodium within the body. In this review, the factors that determine output of sodium and fluid and those that determine "normal" input (i.e., matched to output) are addressed. For output, individual variability accompanied by dysregulation of homeostatic mechanisms may contribute to acute and/or chronic disease. To illustrate that point, the specific condition of salt-sensitive hypertension is discussed. For input, physical characteristics, physiological phenotypes, genetic and developmental influences, and cultural and environmental factors combine to result in a wide range of individual variability that, in humans, is compensated for by alterations in excretion.
维持体内平衡需要对钠和水的摄入与排出进行生理调节。控制液体和盐分平衡的行为及神经内分泌机制高度相互依存，肾脏排出量的急性和慢性变化通过口渴的适当变化以及在较小程度上通过人类的钠食欲得到紧密平衡。在健康个体中，这些紧密耦合的机制通过引发摄食行为以及释放体内保存水和钠所需的激素，将细胞外液体积和身体张力维持在狭窄的体内平衡范围内。在本综述中，探讨了决定钠和液体排出量的因素以及决定“正常”摄入量（即与排出量相匹配）的因素。对于排出量而言，个体差异以及体内平衡机制失调可能导致急性和/或慢性疾病。为说明这一点，讨论了盐敏感性高血压的具体情况。对于摄入量，物理特征、生理表型、遗传和发育影响以及文化和环境因素共同作用，导致了广泛的个体差异，在人类中，这种差异通过排泄的改变得到补偿。
