Silva Marcia S, Lúcio-Oliveira Fabiana, Mecawi Andre Souza, Almeida Lucas F, Ruginsk Silvia G, Greenwood Michael P, Greenwood Mingkwan, Vivas Laura, Elias Lucila L K, Murphy David, Antunes-Rodrigues José
Department of Physiology, School of Medicine of Ribeirao Preto University of Sao Paulo, Ribeirao Preto, São Paulo, Brazil.
Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Physiol Rep. 2017 Mar;5(6). doi: 10.14814/phy2.13210.
Excessive sodium (Na) intake in modern society has been associated with several chronic disorders such as hypertension. Several studies suggest that early life events can program physiological systems and lead to functional changes in adulthood. Therefore, we investigated behavioral and neuroendocrine responses under basal conditions and after 48 h of water deprivation in adult (60-day-old Wistar rats) male, Wistar rats originating from dams were offered only water or 0.15 mol/L NaCl during pregnancy and lactation. Early life salt exposure induced kidney damage, as shown by a higher number of ED-1 positive cells (macrophages/monocytes), increased daily urinary volume and Na excretion, blunted basal water intake and plasma oxytocin levels, and increased plasma corticosterone secretion. When challenged with water deprivation, animals exposed to 0.15 mol/L NaCl during early life showed impaired water intake, reduced salt preference ratio, and vasopressin (AVP) secretion. In summary, our data demonstrate that the perinatal exposure to excessive Na intake can induce kidney injury in adult offspring and significantly affect the key mechanisms regulating water balance, fluid intake, and AVP release in response to water deprivation. Collectively, these novel results highlight the impact of perinatal programming on the homeostatic mechanisms regulating fluid and electrolyte balance during exposure to an environmental stress (i.e. dehydration) in later life.
现代社会中过量的钠（Na）摄入与多种慢性疾病如高血压有关。多项研究表明，早期生活事件可对生理系统进行编程，并导致成年期的功能变化。因此，我们研究了成年（60日龄Wistar大鼠）雄性Wistar大鼠在基础条件下以及48小时禁水后的行为和神经内分泌反应，这些大鼠的母鼠在怀孕和哺乳期仅被提供水或0.15 mol/L NaCl。早期生活中的盐暴露导致肾脏损伤，表现为ED-1阳性细胞（巨噬细胞/单核细胞）数量增加、每日尿量和钠排泄增加、基础水摄入量和血浆催产素水平降低以及血浆皮质酮分泌增加。当受到禁水挑战时，早期生活中暴露于0.15 mol/L NaCl的动物表现出饮水受损、盐偏好率降低和血管加压素（AVP）分泌减少。总之，我们的数据表明，围产期暴露于过量的钠摄入可导致成年后代肾脏损伤，并显著影响调节水平衡、液体摄入以及对禁水反应时AVP释放的关键机制。总体而言，这些新结果突出了围产期编程对成年后暴露于环境应激（即脱水）期间调节液体和电解质平衡的稳态机制的影响。
