McCarty R, Plunkett L M
Brain Res Bull. 1986 Dec;17(6):767-72. doi: 10.1016/0361-9230(86)90088-2.
Binding sites for atrial natriuretic factor (ANF-28) were analyzed in discrete brain areas of Brattleboro rats with hereditary diabetes insipidus and Long-Evans (LE) controls by quantitative autoradiography. The maximum binding capacity (Bmax) and affinity constant (Ka) for 125I-ANF-28 were elevated significantly in the subfornical organ of Brattleboro rats compared to matched LE controls. In contrast, values for Bmax and Ka for 125I-ANF-28 binding in choroid plexus and area postrema were similar for rats of the two strains. These findings are consistent with a selective upregulation of ANF-28 binding sites in the subfornical organ of Brattleboro rats which exhibit a profound disturbance in body fluid homeostasis. These alterations in ANF-28 binding sites in the subfornical organ may represent a compensatory response to the absence of vasopressin in the Brattleboro rat.
通过定量放射自显影技术，分析遗传性尿崩症的布拉特洛维大鼠及作为对照的朗-埃文斯（LE）大鼠离散脑区中心房钠尿肽（ANF-28）的结合位点。与配对的LE对照大鼠相比，布拉特洛维大鼠穹窿下器官中125I-ANF-28的最大结合容量（Bmax）和亲和常数（Ka）显著升高。相比之下，两种品系大鼠脉络丛和最后区中125I-ANF-28结合的Bmax和Ka值相似。这些发现与布拉特洛维大鼠穹窿下器官中ANF-28结合位点的选择性上调一致，这些大鼠在体液稳态方面存在严重紊乱。穹窿下器官中ANF-28结合位点的这些改变可能代表了对布拉特洛维大鼠中抗利尿激素缺乏的一种代偿反应。
