Barac-Nieto M, Dowd T L, Gupta R K, Spitzer A
Department of Pediatrics, Albert Einstein College of Medicine, Bronx, New York 10461.
Am J Physiol. 1991 Jul;261(1 Pt 2):F153-62. doi: 10.1152/ajprenal.1991.261.1.F153.
To test the hypothesis that growth and dietary Pi affect the intracellular concentration of Pi ([Pi]i) as well as its renal reabsorption, we measured nuclear magnetic resonance (NMR)-visible [Pi]i in isolated perfused kidneys of less than 1- and greater than 4-wk-old guinea pigs fed various amounts of Pi. Changes in [Pi]i were correlated with those in fractional Pi reabsorption (FRPi) in vivo and in capacity (Vmax) for Na(+)-Pi cotransport in microvilli derived from animals of similar age and fed the same diets. In animals fed normal (0.76% Pi) diet, [Pi]i was lower (0.91 +/- 0.14 vs. 1.85 +/- 0.23 mM, P less than 0.05), whereas FRPi was higher (0.90 +/- 0.02 vs. 0.70 +/- 0.03, P less than 0.01) in less than 1- than in greater than 4-wk-old guinea pigs. Pi deprivation decreased [Pi]i in mature animals to 0.74 +/- 0.29 mM, P less than 0.05, and increased FRPi to 0.99 +/- 0.01. Excess dietary Pi increased [Pi]i in immature animals to 1.67 +/- 0.56 mM, P less than 0.05, and decreased FRPi to 0.55 +/- 0.03. Diet-induced changes in [Pi]i were associated with reciprocal changes in Vmax of similar absolute magnitude in immature and mature animals. However, diets that resulted in comparable [Pi]i at the two ages were associated with higher (P less than 0.05) Vmax in less than 1- than in greater than 4-wk-old animals. The reciprocal nature of the relationship between [Pi]i and renal Pi transport indicates that [Pi]i is primarily determined by Pi efflux from the cells or Pi organification rather than Pi influx through Na(+)-Pi cotransport. Findings indicate that changes in [Pi]i with growth or diet may be a cause but cannot be the consequence of changes in abundance or maximal mobility of Na(+)-Pi cotransporters. Data also indicate that factors in addition to low [Pi]i contribute to the high Na(+)-Pi cotransport capacity observed in renal microvilli of growing animals.
为了验证生长和膳食磷影响细胞内磷浓度([Pi]i)及其肾脏重吸收这一假说,我们测量了喂食不同量磷的1周龄以下和4周龄以上豚鼠分离灌注肾脏中核磁共振(NMR)可见的[Pi]i。[Pi]i的变化与体内磷重吸收分数(FRPi)的变化以及来自相似年龄且喂食相同饮食的动物微绒毛中钠磷共转运能力(Vmax)的变化相关。在喂食正常(0.76%磷)饮食的动物中,1周龄以下豚鼠的[Pi]i较低(0.91±0.14对1.85±0.23 mM,P<0.05),而FRPi较高(0.90±0.02对0.70±0.03,P<0.01)。磷缺乏使成熟动物的[Pi]i降至0.74±0.29 mM,P<0.05,并使FRPi升至0.99±0.01。过量的膳食磷使未成熟动物的[Pi]i升至1.67±0.56 mM,P<0.05,并使FRPi降至0.55±0.03。饮食诱导的[Pi]i变化与未成熟和成熟动物中Vmax绝对值的反向变化相关。然而,在两个年龄段导致[Pi]i相当的饮食,与1周龄以下动物相比,4周龄以上动物的Vmax更高(P<0.05)。[Pi]i与肾脏磷转运之间关系的反向性质表明,[Pi]i主要由细胞内磷流出或磷有机化决定,而非通过钠磷共转运的磷流入。研究结果表明,[Pi]i随生长或饮食的变化可能是原因,但不是钠磷共转运体丰度或最大转运能力变化的结果。数据还表明,除了低[Pi]i之外的因素也有助于生长动物肾脏微绒毛中观察到的高钠磷共转运能力。