Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats.
Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats.
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血管紧张素 II 与钠负荷和钠耗竭大鼠的肾小球结合。
DOI：
10.1152/ajplegacy.1976.230.5.1187
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
R. Ardaillou
中科院分区：
文献类型：
--
作者：
M. Beaufils;J. Sraer;C. Lepreux;R. Ardaillou
125i标记的血管紧张素II （125I-labeled AII）和[3H]血管紧张素II （[3H]AII）特异性结合离体大鼠肾小球。通过KD值(分别为7.1 +/- 0.3 X 10（- 11,3.4 +/- 0.2 X 10（-10）和1.6 X 10(-9) M）和受体位点数量（分别为11.6 +/- 1.2,29.4 +/- 3.9和113.8 +/- 3.8 fmol/mg肾小球蛋白）可以定义三组受体位点。125i标记AII的缔合常数和解离常数均大于[3H]AII，但两者的比值（KD）保持不变。结合这三组受体位点的特异性通过以下方式证明：1)未标记的激素或拮抗剂抑制标记AII的结合；2)结合的可逆性，不依赖于激素或受体的降解。与急性和慢性钠耗尽大鼠的肾小球制剂相比，急性和慢性钠负荷大鼠的肾小球制剂的结合增加。这种结合的变化是由于受体位点数量的变化和AII对其受体的亲和力的改变。低钠大鼠制剂的KD（慢性和急性低钠大鼠分别为12.9 +/- 3.3和14.6 +/- 3.9 X 10(-11) M）高于高钠大鼠制剂（慢性和急性高钠大鼠分别为2.7 +/- 0.2和3.9 +/- 1 X 10(-11) M）。AII与其肾小球受体结合的改变可能在肾小球滤过率对钠平衡的适应中起作用。
125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Three groups of receptor sites could be defined by the KD value (7.1 +/- 0.3 X 10(-11, 3.4 +/- 0.2 X 10(-10), and 1.6 X 10(-9) M, respectively) and the number of receptor sites (11.6 +/- 1.2, 29.4 +/- 3.9, and 113.8 +/- 3.8 fmol/mg glomerular protein, respectively). Both association and dissociation constants for 125I-labeled AII were greater than those for [3H]AII, but their ratio (KD) remained unchanged. Specificity of binding to these three groups of receptor sites was demonstrated by the following: 1) inhibition of binding of labeled AII by unlabeled hormone or by antagonists; and 2) reversibility of binding, independent of either hormone or receptor degradation. Binding was increased in glomerular preparations from acutely and chronically sodium-loaded rats, compared with glomerular preparations from acutely and chronically sodium-depleted rats. This change in binding resulted from both a change in the number of receptor sites and modification of the affinity of AII for its receptors. KD was higher in preparations from sodium-depleted rats (12.9 +/- 3.3 and 14.6 +/- 3.9 X 10(-11) M in chronically and acutely depleted rats, respectively) than in those from sodium-loaded rats (2.7 +/- 0.2 and 3.9 +/- 1 X 10(-11) M in chronically and acutely sodium-loaded rats, respectively). Changes in the binding of AII to its glomerular receptors could play a role in the adaptation of glomerular filtration rate to the sodium balance.