PARATHYROID-HORMONE ACTION ON PHOSPHATE TRANSPORTER MESSENGER-RNA AND PROTEIN IN RAT RENAL PROXIMAL TUBULES

被引:165
作者
KEMPSON, SA
LOTSCHER, M
KAISSLING, B
BIBER, J
MURER, H
LEVI, M
机构
[1] INDIANA UNIV, MED CTR, DEPT PHYSIOL & BIOPHYS, INDIANAPOLIS, IN 46223 USA
[2] UNIV ZURICH, INST PHYSIOL & ANAT, CH-8057 ZURICH, SWITZERLAND
[3] UNIV TEXAS, SW MED CTR, DEPT INTERNAL MED, DALLAS, TX 75216 USA
[4] VET AFFAIRS MED CTR, DALLAS, TX 75216 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY | 1995年 / 268卷 / 04期
关键词
PHOSPHATE TRANSPORT; CELLULAR REGULATION; ENDOCYTOSIS; NAPI-2; KIDNEY;
D O I
10.1152/ajprenal.1995.268.4.F784
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The inhibitory action of parathyroid hormone (PTH) on P-i reabsorption in the renal proximal tubule is accompanied by a specific decrease in Na-P-i cotransport at the apical brush-border membrane (BBM). It is not known whether this decrease represents decreased activity of Na-P-i cotransporters already present in the BBM or whether the number of cotransporters is decreased. The present study of the molecular mechanism of PTH action made use of a specific cDNA probe and antiserum to a rat renal Na-P-i cotransporter (NaPi-2). Three groups of rats were used: intact controls, chronically parathyroidectomized (PTX), and PTX rats treated acutely (2 h) with bovine PTH-(1-34). Na-P-i cotransport by isolated renal BBM vesicles was increased to 1,315 +/- 44 in PTX rats, compared with 721 +/- 94 pmol . mg(-1). 10 s(-1) in controls (P < 0.002), and was returned to control levels by PTH. Western blots of these BBM showed that PTX caused a 2.8-fold increase in NaPi-2 protein content, which was reduced to control levels by PTH. Immunohistochemistry of perfusion-fixed kidneys showed NaPi-2-specific immunofluorescence exclusively in apical BBM of proximal tubules. Expression of NaPi-2 protein at these sites was increased in PTX rats and decreased after PTH treatment. Northern analysis of total RNA showed that the abundance of NaPi-2-specific mRNA was not changed by PTX but there was a small decrease in response to PTH. The data indicate that PTH regulation of renal Na-Pi cotransport is determined by changes in expression of NaPi-2 protein in the renal BBM. PTH may decrease the NaPi-2 protein content of BBM in part by a mechanism that results in endocytic withdrawal into a cytoplasmic pool.
引用
收藏
页码:F784 / F791
页数:8
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