Differential regulation of angiotensin II receptor subtypes in rat kidney by low dietary sodium.
Differential regulation of angiotensin II receptor subtypes in rat kidney by low dietary sodium.
复制标题
低钠饮食对大鼠肾脏血管紧张素 II 受体亚型的差异调节。
DOI:
10.1161/01.hyp.25.4.872
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发表时间:
1995
期刊:
影响因子:
--
通讯作者:
Wang,DH
中科院分区:
文献类型:
--
作者:
Du,Y;Yao,A;Guo,D;Inagami,T;Wang,DH
This study was designed to determine whether expression of renal messenger RNA (mRNA) encoding the two known angiotensin II type 1 (AT1) receptor subtypes (AT1Aand AT1B) can be regulated by dietary sodium. Seven-week-old male Wistar rats were fed a low-sodium diet (0.07%, n=9) or a normal-sodium diet (0.5%, n=9 [control]) for 14 days. A rat AT1complementary DNA (cDNA) probe, which hybridizes to mRNA encoding both the AT1Aand AT1Breceptor subtypes, and cDNA probes, which are selective for AT1Aor AT1BmRNA, were used in Northern blot or in situ hybridization analysis. By use of Northern blot analysis, renal mRNA levels for the AT1and AT1Areceptors in rats fed a low-sodium diet were found to be increased twofold (P<.05) compared with control. Because renal AT1BmRNA content was not detected by Northern blot analysis, quantitative image analysis of in situ hybridization with a digoxigenin-labeled cRNA probe made from AT1BcDNA was used. In situ hybridization analysis indicated that AT1BmRNA was expressed in the proximal and collecting tubules of the kidney in rats fed a normal-sodium diet. The low-sodium diet significantly decreased the percent positive staining area of AT1BmRNA in the renal cortex (5.51±0.77% versus 2.73±0.35%,P<.05) and medulla (4.76±0.70% versus 2.01±0.43%,P<.05) compared with the control diet. These results indicate that the increase in AT1mRNA levels in the kidney induced by low sodium intake is the result of a selective increase in AT1AmRNA and suggest that AT1Ais the predominant receptor subtype of AT1in the kidney. The data also suggest that dietary sodium differentially modulates the expression of genes encoding AT1receptor subtypes, because there is an inverse relationship between the expression of the AT1Aand AT1Bsubtypes in response to a low-sodium diet. The functional implications are discussed.