Departamento de Fisiología, Facultad de Medicina, Granada, Spain.
Am J Physiol Endocrinol Metab. 2011 Aug;301(2):E281-7. doi: 10.1152/ajpendo.00690.2010. Epub 2011 Apr 26.
This study assessed salt sensitivity, analyzing the effects of an increased saline intake on hemodynamic, morphological, and oxidative stress and renal variables in experimental thyroid disorders. Six groups of male Wistar rats were used: control, hypothyroid, hyperthyroid, and the same groups treated with salt (8% via food intake). Body weight, blood pressure (BP), and heart rate (HR) were recorded weekly for 6 wk. Finally, BP and HR were recorded directly, and morphological, metabolic, plasma, and renal variables were measured. High-salt intake increased BP in thyroxine-treated rats but not in control or hypothyroid rats. High-salt intake increased cardiac mass in all groups, with a greater increase in hyperthyroid rats. Urinary isoprostanes and H(2)O(2) were higher in hyperthyroid rats and were augmented by high-salt intake in all groups, especially in hyperthyroid rats. High-salt intake reduced plasma thyroid hormone levels in hyperthyroid rats. Proteinuria was increased in hyperthyroid rats and aggravated by high-salt intake. Urinary levels of aminopeptidases (glutamyl-, alanyl-, aspartyl-, and cystinylaminopeptidase) were increased in hyperthyroid rats. All aminopeptidases were increased by salt intake in hyperthyroid rats but not in hypothyroid rats. In summary, hyperthyroid rats have enhanced salt sensitivity, and high-salt intake produces increased BP, cardiac hypertrophy, oxidative stress, and signs of renal injury. In contrast, hypothyroid rats are resistant to salt-induced BP elevation and renal injury signs. Urinary aminopeptidases are suitable biomarkers of renal injury.
本研究评估了盐敏感性，分析了增加盐摄入量对甲状腺功能障碍实验模型的血流动力学、形态学和氧化应激及肾脏变量的影响。使用了六组雄性 Wistar 大鼠：对照组、甲状腺功能减退组、甲状腺功能亢进组和同样给予盐（通过食物摄入 8%）治疗的三组。每周记录体重、血压（BP）和心率（HR），共 6 周。最后直接记录 BP 和 HR，并测量形态学、代谢、血浆和肾脏变量。高盐摄入增加了甲状腺素治疗大鼠的血压，但对对照组或甲状腺功能减退大鼠没有影响。高盐摄入增加了所有组的心脏质量，甲状腺功能亢进大鼠的增加更为明显。所有组的尿 8-异前列腺素和 H2O2 均升高，且高盐摄入进一步增加，甲状腺功能亢进大鼠增加更为明显。高盐摄入降低了甲状腺功能亢进大鼠的血浆甲状腺激素水平。甲状腺功能亢进大鼠的蛋白尿增加，并因高盐摄入而加重。甲状腺功能亢进大鼠的尿氨肽酶（谷氨酰氨肽酶、丙氨酰氨肽酶、天冬氨酰氨肽酶和胱氨酰氨肽酶）水平升高。所有氨肽酶在甲状腺功能亢进大鼠中因盐摄入而增加，但在甲状腺功能减退大鼠中没有增加。总之，甲状腺功能亢进大鼠对盐更为敏感，高盐摄入导致 BP 升高、心脏肥大、氧化应激和肾脏损伤迹象增加。相反，甲状腺功能减退大鼠对盐诱导的 BP 升高和肾脏损伤迹象有抵抗力。尿氨肽酶是肾脏损伤的合适生物标志物。
