Developmental changes in renal tubular transport-an overview

被引:40
作者
Gattineni, Jyothsna [1 ]
Baum, Michel [1 ]
机构
[1] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA
基金
美国国家卫生研究院;
关键词
Renal development; Sodium transport; Nephron; Ontogeny of renal transport; RABBIT PROXIMAL TUBULE; URINARY CONCENTRATING CAPACITY; NA-K-ATPASE; INHERITED HYPOKALEMIC ALKALOSIS; CORTICAL COLLECTING DUCT; ANHYDRASE-IV EXPRESSION; THYROID-HORMONE; POSTNATAL MATURATION; NA+/H+ ANTIPORTER; MESSENGER-RNA;
D O I
10.1007/s00467-013-2666-6
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The adult kidney maintains a constant volume and composition of extracellular fluid despite changes in water and salt intake. The neonate is born with a kidney that has a small fraction of the glomerular filtration rate of the adult and immature tubules that function at a lower capacity than that of the mature animal. Nonetheless, the neonate is also able to maintain a constant extracellular fluid volume and composition. Postnatal renal tubular development was once thought to be due to an increase in the transporter abundance to meet the developmental increase in glomerular filtration rate. However, postnatal renal development of each nephron segment is quite complex. There are isoform changes of several transporters as well as developmental changes in signal transduction that affect the capacity of renal tubules to reabsorb solutes and water. This review will discuss neonatal tubular function with an emphasis on the differences that have been found between the neonate and adult. We will also discuss some of the factors that are responsible for the maturational changes in tubular transport that occur during postnatal renal development.
引用
收藏
页码:2085 / 2098
页数:14
相关论文
共 164 条
[31]   SLC34A3 mutations in patients with hereditary hypophosphatemic rickets with hypercalciuria predict a key role for the sodium-phosphate cotransporter NaPi-IIc in maintaining phosphate homeostasis [J].
Bergwitz, C ;
Roslin, NM ;
Tieder, M ;
Loredo-Osti, JC ;
Bastepe, M ;
Abu-Zahra, H ;
Frappier, D ;
Burkett, K ;
Carpenter, O ;
Anderson, D ;
Garabédian, M ;
Sermet, I ;
Fujiwara, TM ;
Morgan, K ;
Tenenhouse, HS ;
Jüppner, H .
AMERICAN JOURNAL OF HUMAN GENETICS, 2006, 78 (02) :179-192
[32]   PROSTAGLANDINS MEDIATE THE DEFECT IN AVP-STIMULATED CAMP GENERATION IN IMMATURE COLLECTING DUCT [J].
BONILLAFELIX, M ;
JOHNPHILLIP, C .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 267 (01) :F44-F48
[33]   Postnatal expression of transport proteins involved in acid-base transport in mouse kidney [J].
Bonnici, B ;
Wagner, CA .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 2004, 448 (01) :16-28
[34]   CHANGES IN SOLUBLE CARBONIC-ANHYDRASE ACTIVITY IN RESPONSE TO MATURATION AND NH4CL LOADING IN THE RABBIT [J].
BRION, LP ;
ZAVILOWITZ, BJ ;
ROSEN, O ;
SCHWARTZ, GJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (05) :R1204-R1213
[35]   Acute ENaC stimulation by cAMP in a kidney cell line is mediated by exocytic insertion from a recycling channel pool [J].
Butterworth, MB ;
Edinger, RS ;
Johnson, JP ;
Frizzell, RA .
JOURNAL OF GENERAL PHYSIOLOGY, 2005, 125 (01) :81-101
[36]   Regulation of the epithelial sodium channel by membrane trafficking [J].
Butterworth, Michael B. ;
Edinger, Robert S. ;
Frizzell, Raymond A. ;
Johnson, John P. .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2009, 296 (01) :F10-F24
[37]   Thyroid hormone stimulates the renal Na/H exchanger NHE3 by transcriptional activation [J].
Cano, A ;
Baum, M ;
Moe, OW .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1999, 276 (01) :C102-C108
[38]  
CAVERZASIO J, 1982, AM J PHYSIOL, V242, pF705, DOI 10.1152/ajprenal.1982.242.6.F705
[39]   ABUNDANCE OF NA+-K+-ATPASE MESSENGER-RNA IS REGULATED BY GLUCOCORTICOID HORMONES IN INFANT RAT KIDNEYS [J].
CELSI, G ;
NISHI, A ;
AKUSJARVI, G ;
APERIA, A .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (02) :F192-F197
[40]   Novel amiloride-sensitive sodium-dependent proton secretion in the mouse proximal convoluted tubule [J].
Choi, JY ;
Shah, M ;
Lee, MG ;
Schultheis, PJ ;
Shull, GE ;
Muallem, S ;
Baum, M .
JOURNAL OF CLINICAL INVESTIGATION, 2000, 105 (08) :1141-1146