TY - JOUR
T1 - Phylogenetic, ontogenetic, and pathological aspects of the urine-concentrating mechanism
AU - Kondo, Yoshiaki
AU - Morimoto, Tetsuji
AU - Nishio, Toshiyuki
AU - Aslanova, Ulviyya Fizuli
AU - Nishino, Minako
AU - Farajov, Elnur Ilham
AU - Sugawara, Noriko
AU - Kumagai, Naonori
AU - Ohsaga, Atsushi
AU - Maruyama, Yoshio
AU - Takahashi, Shori
PY - 2006/9
Y1 - 2006/9
N2 - The urine-concentrating mechanism is one of the most fundamental functions of avian and mammalian kidneys. This particular function of the kidneys developed as a system to accumulate NaCl in birds and as a system to accumulate NaCl and urea in mammals. Based on phylogenetic evidence, the mammalian urine-concentrating mechanism may have evolved as a modification of the renal medulla's NaCl accumulating system that is observed in birds. This qualitative conversion of the urine-concentrating mechanism in the mammalian inner medulla of the kidneys may occur during the neonatal period. Human kidneys have several suboptimal features caused by the neonatal conversion of the urine-concentrating mechanism. The urine-concentrating mechanism is composed of various functional molecules, including water channels, solute transporters, and vasopressin receptors. Abnormalities in water channels aquaporin (AQP)1 and AQP2, as well as in the vasopressin receptor V2R, are known to cause nephrogenic diabetes insipidus. An analysis of the pathological mechanism involved in nephrogenic diabetes insipidus suggests that molecular chaperones may improve the intracellular trafficking of AQP2 and V2R, and, in the near future, such chaperones may become a new clinical tool for treating nephrogenic diabetes insipidus.
AB - The urine-concentrating mechanism is one of the most fundamental functions of avian and mammalian kidneys. This particular function of the kidneys developed as a system to accumulate NaCl in birds and as a system to accumulate NaCl and urea in mammals. Based on phylogenetic evidence, the mammalian urine-concentrating mechanism may have evolved as a modification of the renal medulla's NaCl accumulating system that is observed in birds. This qualitative conversion of the urine-concentrating mechanism in the mammalian inner medulla of the kidneys may occur during the neonatal period. Human kidneys have several suboptimal features caused by the neonatal conversion of the urine-concentrating mechanism. The urine-concentrating mechanism is composed of various functional molecules, including water channels, solute transporters, and vasopressin receptors. Abnormalities in water channels aquaporin (AQP)1 and AQP2, as well as in the vasopressin receptor V2R, are known to cause nephrogenic diabetes insipidus. An analysis of the pathological mechanism involved in nephrogenic diabetes insipidus suggests that molecular chaperones may improve the intracellular trafficking of AQP2 and V2R, and, in the near future, such chaperones may become a new clinical tool for treating nephrogenic diabetes insipidus.
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U2 - 10.1007/s10157-006-0429-4
DO - 10.1007/s10157-006-0429-4
M3 - Review article
C2 - 17009073
AN - SCOPUS:33749363986
SN - 1342-1751
VL - 10
SP - 165
EP - 174
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
IS - 3
ER -