Iwai J, Knudsen K D, Dahl L K, Tassinari L
J Exp Med. 1969 Apr 1;129(4):663-78. doi: 10.1084/jem.129.4.663.
In adrenalectomized, genetically hypertension-prone rats, a high degree of correlation was found between evidence of functioning adrenal tissue and the development of salt hypertension. There is considerable evidence that some rats have the capacity to regenerate functioning adrenal cortical tissue from accessory glands and microscopic rests, sometimes in remote locations. Therefore, the criteria for continued absence of adrenal function after surgical adrenalectomy are critical. In this study we used three tests to validate the presence, or absence, of adrenal function: (a) a biochemical test, the quantitative, serial measurement of plasma glucocorticoids in individual rats; (b) a physiological test, the ability to survive a virtually sodium-free diet; and (c) the anatomical search for histological evidence of adrenal cortical tissue. Among those animals that developed hypertension after adrenalectomy, the correlation between plasma steroid concentration and blood pressure was statistically significant. We suspect that this correlation exists only during the period when cortical tissue is regenerating; it does not exist among intact animals with and without hypertension induced by salt. It was concluded that some adrenocortical function is necessary for salt hypertension to develop. The evidence was insufficient to settle the question whether the action of corticosteroids is causative, or whether they play a supporting, although necessary, role for an extraadrenal hypertensinogenic factor to become manifest.
在肾上腺切除的、具有遗传性高血压倾向的大鼠中,发现有功能的肾上腺组织证据与盐性高血压的发展之间存在高度相关性。有大量证据表明,一些大鼠有能力从副腺体和微小残余组织中再生出有功能的肾上腺皮质组织,有时这些组织位于较远的位置。因此,手术切除肾上腺后持续无肾上腺功能的标准至关重要。在本研究中,我们使用了三项测试来验证肾上腺功能的有无:(a) 一项生化测试,即对个体大鼠血浆糖皮质激素进行定量、连续测量;(b) 一项生理测试,即耐受几乎无钠饮食的能力;(c) 对肾上腺皮质组织的组织学证据进行解剖学查找。在肾上腺切除后发生高血压的那些动物中,血浆类固醇浓度与血压之间的相关性具有统计学意义。我们怀疑这种相关性仅存在于皮质组织再生期间;在有盐诱导高血压和无盐诱导高血压的完整动物中并不存在。得出的结论是,某种肾上腺皮质功能对于盐性高血压的发展是必要的。证据不足以确定皮质类固醇的作用是病因性的,还是它们只是为肾上腺外的高血压生成因子发挥作用提供支持,尽管这种支持是必要的。