Graduate Program of Translational Biomedicine/BIOTRANS, University of Grande Rio, Duque de Caxias, Brazil.
Leopoldo de Meis Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
PLoS One. 2022 Aug 19;17(8):e0273385. doi: 10.1371/journal.pone.0273385. eCollection 2022.
We investigated the mechanisms by which chronic administration of a multideficient diet after weaning alters bodily Na+ handling, and culminates in high systolic blood pressure (SBP) at a juvenile age. From 28 to 92 days of age, weaned male Wistar rats were given a diet with low content and poor-quality protein, and low lipid, without vitamin supplementation, which mimics the diets consumed in impoverished regions worldwide. We measured food, energy and Na+ ingestion, together with urinary Na+ excretion, Na+ density (Na+ intake/energy intake), plasma Na+ concentration, SBP, and renal proximal tubule Na+-transporting ATPases. Undernourished rats aged 92 days had only one-third of the control body mass, lower plasma albumin, higher SBP, higher energy intake, and higher positive Na+ balance accompanied by decreased plasma Na+ concentration. Losartan or Ang-(3-4) normalized SBP, and the combination of the 2 substances induced an accentuated negative Na+ balance as a result of strong inhibition of Na+ ingestion. Na+ density in undernourished rats was higher than in control, irrespective of the treatment, and they had downregulated (Na++K+)ATPase and upregulated Na+-ATPase in proximal tubule cells, which returned to control levels after Losartan or Ang-(3-4). We conclude that Na+ density, not only Na+ ingestion, plays a central role in the pathophysiology of elevated SBP in chronically undernourished rats. The observations that Losartan and Ang-(3-4) normalized SBP together with negative Na+ balance give support to the proposal that Ang II⇒AT1R and Ang II⇒AT2R axes have opposite roles within the renin-angiotensin-aldosterone system of undernourished juvenile rats.
我们研究了断奶后长期给予多种缺乏饮食的机制,这些机制改变了身体的钠处理方式,并最终导致青少年时期的收缩压(SBP)升高。从 28 到 92 天龄,我们给断奶的雄性 Wistar 大鼠喂食低含量和低质量蛋白质、低脂肪、不含维生素补充剂的饮食,这种饮食模仿了世界各地贫困地区的饮食。我们测量了食物、能量和钠摄入以及尿钠排泄、钠密度(钠摄入量/能量摄入量)、血浆钠浓度、SBP 和肾近端小管钠转运 ATP 酶。92 天大的营养不良大鼠的体重只有对照组的三分之一,血浆白蛋白水平较低,SBP 较高,能量摄入较高,正钠平衡较高,同时血浆钠浓度降低。Losartan 或 Ang-(3-4) 可使 SBP 正常化,两种物质的组合会因强烈抑制钠摄入而导致更明显的负钠平衡。无论治疗如何,营养不良大鼠的钠密度都高于对照组,并且它们的近端肾小管细胞中的(Na++K+)ATP 酶下调,Na+-ATP 酶上调,而 Losartan 或 Ang-(3-4) 后恢复到对照组水平。我们得出结论,钠密度,而不仅仅是钠摄入,在慢性营养不良大鼠的 SBP 升高的病理生理学中起着核心作用。Losartan 和 Ang-(3-4) 使 SBP 正常化和负钠平衡的观察结果支持这样的观点,即 Ang II ⇒ AT1R 和 Ang II ⇒ AT2R 轴在营养不良的幼年大鼠的肾素-血管紧张素-醛固酮系统中具有相反的作用。