Aguilera G, Schirar A, Baukal A, Catt K J
Nature. 1981 Feb 5;289(5797):507-9. doi: 10.1038/289507a0.
Mineralocorticoid secretion is predominantly controlled by the octapeptide angiotensin II, which exerts trophic actions on the adrenal glomerulosa and acute regulatory effects on aldosterone biosynthesis. The trophic actions include stimulation of angiotensin II receptors and enzymes of the aldosterone biosynthetic pathway, with corresponding enhancement of the aldosterone secretory capacity of the adrenal gland. The positive regulatory action of angiotensin II on its adrenal receptors occurs with elevations of the circulating peptide concentration within the physiological range and probably contributes to the increased sensitivity of the adrenal during sodium deficiency. In this action, angiotensin II differs from other hormones which decrease their target-cell receptors. However, the increase in adrenal angiotensin II receptors following nephrectomy has been interpreted as evidence for a tonic down-regulating effect of angiotensin II on its adrenal receptors. To clarify these conflicting views we evaluated the effects of nephrectomy on adrenal angiotensin II receptors in relation to blood angiotensin II and plasma electrolyte levels. We show here that hyperkalaemia contributes markedly to the post-nephrectomy increase in adrenal angiotensin II receptors, and that circulating angiotensin II levels persist for an unexpectedly long period after nephrectomy, presumably due to tissue generation of the octapeptide.
盐皮质激素的分泌主要受八肽血管紧张素II的控制，血管紧张素II对肾上腺球状带发挥营养作用，并对醛固酮的生物合成产生急性调节作用。这些营养作用包括刺激血管紧张素II受体和醛固酮生物合成途径中的酶，相应增强肾上腺的醛固酮分泌能力。血管紧张素II对其肾上腺受体的正向调节作用发生在循环肽浓度在生理范围内升高时，可能有助于钠缺乏时肾上腺敏感性的增加。在这一作用中，血管紧张素II与其他使靶细胞受体减少的激素不同。然而，肾切除术后肾上腺血管紧张素II受体的增加被解释为血管紧张素II对其肾上腺受体存在紧张性下调作用的证据。为了阐明这些相互矛盾的观点，我们评估了肾切除术对肾上腺血管紧张素II受体的影响，并将其与血中血管紧张素II和血浆电解质水平相关联。我们在此表明，高钾血症对肾切除术后肾上腺血管紧张素II受体的增加有显著贡献，并且肾切除术后循环血管紧张素II水平会持续一段意想不到的长时间，推测是由于该八肽的组织生成。
