摘要
文章报道了代谢性酸中毒时大鼠肾组织两种钠离子依赖的枸橼酸膜转运蛋白mRNA表达量的变化。给雌性Wistar大鼠喂含 0 2 8mol/LNH4Cl饮用水诱导产生代谢性酸中毒。喂酸后分别于 1、3、7d处死大鼠 ,测定血浆HCO 3浓度的变化。以Northern杂交方法 ,用钠离子依赖的枸橼酸膜转运蛋白 1(SDCT1)探针及钠离子依赖的枸橼酸膜转运蛋白 2 (SDCT2 )探针 ,分别检测肾皮质枸橼酸转运蛋白mRNA的表达变化。结果显示 ,喂酸后第 1天大鼠血浆内HCO 3浓度明显下降 ,与对照组比较差异显著 (P <0 0 1) ,但Northern杂交结果显示肾小管上皮细胞两侧的枸橼酸转运蛋白mRNA表达量无明显变化。第 3天 ,喂酸组大鼠血浆HCO 3浓度有所回升 ,但仍显著低于对照组 (P <0 0 1) ,肾小管上皮细胞刷状缘侧和基底侧膜的枸橼酸转运蛋白mRNA表达量均明显增加。第 7天喂酸组大鼠血浆HCO 3浓度继续回升 ,与对照组比较无显著差异 (P >0 0 5 ) ,肾小管上皮细胞两侧的枸橼酸转运蛋白mR NA表达仍明显增强。结果提示 ,在代谢性酸中毒时 ,大鼠肾小管上皮细胞两侧钠离子依赖的枸橼酸膜转运蛋白mRNA表达量增加 ,肾脏对枸橼酸的重吸收能力可能增强。
The purpose of the present study was to examine whether metabolic acidosis affects the ex^pression of rat renal Na +/citrate cotransporter. Female Wistar rats were pair fed with normal rat chow and drinking water (control) or water with 0 28 mol/L NH 4Cl (metabolic acidosis). The mRNA of two renal Na +/citrate cotransporters, which were respectively expressed on apical and basolateral membrane, were measured by Northern blot with two probes, SDCT1 and SDCT2. Animals were sacrificed on day 1,3 and 7. On the 1st day, the blood plasma HCO 3 of acidosis group decreased significantly ( P <0 01), but the mRNA abundance did not change. On the 3rd day in the acidosis group, the blood plasma HCO 3 increased slightly more than that on the 1st day, but was still significantly lower than that of the control group ( P <0 01). Both the probes detected some increase in mRNA of brush border and basolateral Na +/citrate cotrans^porter. On the 7th day, the blood plasma HCO 3 of the acidosis group continuously increased and there was no significant difference between the two groups. The abundance of brush border and basolateral Na +/citrate cotransporter mRNA increased, but there was no difference between those of the 3rd day and the 7th day. It is concluded that metabolic acidosis can induce increase of Na +/citrate cotransporter mRNA, which may be responsible for hypocitraturia.
出处
《生理学报》
CAS
CSCD
北大核心
2000年第1期55-58,共4页
Acta Physiologica Sinica
基金
SupportedbytheNationalNaturalScienceFoundationofChina !(No 39870 32 3)
