Renal receptors and effects of atrial natriuretic factor in compensatory renal hypertrophy.
Renal receptors and effects of atrial natriuretic factor in compensatory renal hypertrophy.
复制标题
肾受体和心房钠尿因子在代偿性肾肥大中的作用。
DOI：
10.1038/ki.1992.263
复制
发表时间：
1992
影响因子：
19.6
通讯作者：
Maack,T
中科院分区：
文献类型：
--
作者：
Price,DA;Okolicany,J;Maack,T
Renal receptors and effects of atrial natriuretic factor in compensatory renal hypertrophy. In the present study we investigated the in vivo and in vitro renal responsiveness to ANF, and the adaptation of ANF receptors in compensatory renal hypertrophy in the rat. One week after left nephrectomy (UNx), plasma levels of immunoreactive ANF, blood pressure (MAP), hematocrit (Hct), and urine flow rate (V) were unaltered compared to control (C) rats. Baseline GFR and potassium excretion (UKV) were significantly higher, and sodium excretion (UNaV) tended to be elevated in UNx rats. Administered ANF led to similar dose-related decreases in MAP and increases in Hct in UNx and C rats. However, at each dose of infused ANF, absolute values and the increase in GFR and UNaV were higher in UNx than in C rats. Hypertrophied (H) kidneys were removed from UNx and perfused in vitro to determine distribution and density of ANF receptors, responsiveness to ANF, and receptor-mediated organ clearance of125I-ANF1-28. The density of ANF receptors in cortex, outer medulla, and papilla of H kidneys was not significantly different from that in C kidneys. In H isolated kidneys, ANF led to dose-related increases in GFR, V, UNaV, and UKV that were indistinguishable (P > 0.05) from those in C kidneys. Receptor-mediated organ clearance of125I-ANF1-28in isolated H kidneys was 2.8 ± .02 ml/min, a value not significantly different (P > 0.05) from that in C kidneys. The results demonstrate that the number of renal receptors of ANF increases in proportion to kidney weight in compensatory hypertrophy, leading to a normal intrarenal distribution and receptor density, as well as preserved responsiveness to ANF and receptor-mediated clearance of the hormone. This adaptation, together with systemic factors that lead to the enhanced responsiveness to ANF in vivo, may contribute importantly to the preservation of sodium volume homeostasis in compensatory hypertrophy.
