Bonilla-Felix Melvin
Department of Pediatrics, Univerity of Puerto Rico-Medical Sciences, Campus, San Juan, PR 00936-5067.
Am J Physiol Renal Physiol. 2004 Dec;287(6):F1093-101. doi: 10.1152/ajprenal.00119.2004.
The ability of the immature kidney to concentrate urine is lower than in adults. This can lead to severe water and electrolyte disorders, especially in premature babies. Resistance to AVP and lower tonicity of the medullary interstitium seem to be the major factors limiting urine concentration in newborns. AVP-stimulated cAMP generation is impaired. This is the result of inhibition of the production by PGE(2) acting through EP3 receptors and increased degradation by phosphodiesterase IV. The expression of aquaporin-2 (AQP2) in the immature kidney is low; however, under conditions of water deprivation and after stimulation with DDAVP, it rises to adult levels. The expression of AQP3 and AQP4 is intact at birth and does not seem to contribute to the hyporesponsiveness to AVP. Low sodium transport by thick ascending loops of Henle, immaturity of the medullary architecture, and adaptations in the transport of urea contribute to the lower tonicity of the medullary interstitium. This paper reviews the alterations in the AVP signal transduction pathway in the immature kidney.
未成熟肾脏浓缩尿液的能力低于成年人。这可能导致严重的水和电解质紊乱，尤其是在早产儿中。对血管加压素（AVP）的抵抗以及髓质间质较低的张力似乎是限制新生儿尿液浓缩的主要因素。AVP刺激的环磷酸腺苷（cAMP）生成受损。这是由于前列腺素E2（PGE(2)）通过EP3受体作用抑制其生成以及磷酸二酯酶IV使其降解增加所致。未成熟肾脏中 aquaporin-2（AQP2）的表达较低；然而，在缺水条件下以及用去氨加压素（DDAVP）刺激后，其表达会升至成人水平。AQP3和AQP4的表达在出生时是完整的，似乎与对AVP反应低下无关。髓袢升支粗段的低钠转运、髓质结构的不成熟以及尿素转运的适应性变化导致髓质间质张力较低。本文综述了未成熟肾脏中AVP信号转导途径的改变。
