Montiel M, Jiménez E, Narváez J A, Morell M
Endocr Res Commun. 1982;9(3-4):249-60. doi: 10.3109/07435808209045768.
A study was made of the responses of the renin-angiotensin-aldosterone system (RAAS) produced in hyper- and hypothyroid rats maintained in a state of sodium depletion, as part of a wider study to effect a comparison with results previously obtained for the same parameters in rats maintained on a normal sodium diet and during experimental alterations of thyroid function. In hyperthyroid rats maintained on sodium deficient and normal sodium diet, and in euthyroid animals on a sodium deficient regimen, elevations of both plasma renin concentration (PRC) and serum aldosterone concentration (AC) were observed, while the plasma renin substrate (PRS) was decreased. In hypothyroid rats with normal sodium intake, PRC and AC were observed to be decreased relative to similar sodium-deficient animals. Relationships were observed between PRC and AC, and between AC and urinary sodium excretion. These results suggest that: i) Sodium depletion is a more effective stimulus than the thyroid hormones on the RAAS. ii) Aldosterone changes in sodium depletion are mediated by the RAS. iii) Sodium depletion appeared to induce a decrease in the hepatic synthesis of angiotensinogen.
作为一项更广泛研究的一部分，该研究观察了处于钠缺乏状态的甲状腺功能亢进和减退大鼠体内肾素 - 血管紧张素 - 醛固酮系统（RAAS）的反应，以便与之前在正常钠饮食的大鼠以及甲状腺功能发生实验性改变期间所获得的相同参数结果进行比较。在维持低钠和正常钠饮食的甲状腺功能亢进大鼠以及处于低钠饮食方案的甲状腺功能正常动物中，观察到血浆肾素浓度（PRC）和血清醛固酮浓度（AC）均升高，而血浆肾素底物（PRS）降低。在钠摄入量正常的甲状腺功能减退大鼠中，相对于类似的钠缺乏动物，PRC和AC降低。观察到PRC与AC之间以及AC与尿钠排泄之间存在相关性。这些结果表明：i）钠缺乏对RAAS的刺激比甲状腺激素更有效。ii）钠缺乏时醛固酮的变化由肾素 - 血管紧张素系统介导。iii）钠缺乏似乎会导致肝脏中血管紧张素原合成减少。
