Toshikazu Saito

Lack of vasopressin-independent upregulation of AQP-2 gene expression in homozygous Brattleboro rats.

Arginine vasopressin (AVP) plays an important role in the expression of aquaporin (AQP-2) in the collecting duct. The present study was undertaken to determine whether there is an AVP-independent regulation of AQP-2 gene expression in homozygous Brattleboro rats in which endogenous AVP is absent. Exogenous administration of 1-deamino-8-d-AVP produced an antidiuresis and expressed AQP-2 mRNA and AQP-2 protein in the renal medulla of the homozygous Brattleboro rats. Twelve hours of water deprivation produced severe dehydration in the homozygous Brattleboro rats, such that urinary osmolality increased from 200 to 649 mosmol/kgH2O. However, no increase in AQP-2 mRNA expression was observed after this dehydration, and the medullary tissue content and urinary excretion of AQP-2 also remained unchanged. Increases in AQP-2 mRNA expression and AQP-2 protein were evident in Long-Evans rats after 64 h of water deprivation, with a severity of dehydration almost equal to the 12-h dehydrated, homozygous Brattleboro rats. These results indicate the lack of an AVP-independent mechanism for upregulating AQP-2 mRNA expression in renal collecting duct cells.Arginine vasopressin (AVP) plays an important role in the expression of aquaporin (AQP-2) in the collecting duct. The present study was undertaken to determine whether there is an AVP-independent regulation of AQP-2 gene expression in homozygous Brattleboro rats in which endogenous AVP is absent. Exogenous administration of 1-deamino-8-D-AVP produced an antidiuresis and expressed AQP-2 mRNA and AQP-2 protein in the renal medulla of the homozygous Brattleboro rats. Twelve hours of water deprivation produced severe dehydration in the homozygous Brattleboro rats, such that urinary osmolality increased from 200 to 649 mosmol/kgH(2)O. However, no increase in AQP-2 mRNA expression was observed after this dehydration, and the medullary tissue content and urinary excretion of AQP-2 also remained unchanged. Increases in AQP-2 mRNA expression and AQP-2 protein were evident in Long-Evans rats after 64 h of water deprivation, with a severity of dehydration almost equal to the 12-h dehydrated, homozygous Brattleboro rats. These results indicate the lack of an AVP-independent mechanism for upregulating AQP-2 mRNA expression in renal collecting duct cells.

Urinary excretion of the aquaporin-2 water channel exaggerated in pathological states of impaired water excretion.

OBJECTIVE The present study was undertaken to determine whether the hydro‐osmotic action of arginine vasopressin (AVP) is exaggerated in pathological states of impaired water excretion by measuring urinary excretion of the aquaporin‐2 (AQP‐2) water channel.

Prompt and Sustained Regulation of Aquaporin-2 by Arginine Vasopressin in Collecting Duct Cells and Clinical Implication of Urinary Excretion of Aquaporin-2

In response to arginine vasopressin (AVP) concentrated urine is produced by water reabsorption across renal collecting duct cells (1). Sasaki et al (2,3) recently cloned a cDNA of apical collecting duct water channel, aquaporin-2 (AQP-2) of the rat and human kidney. AQP-2 are present in the membrane of cytoplasmic vesicles of collecting duct cells, and are translocated to the apical membrane when the cells are stimulated by AVP (4–7). These findings are predicted by “the shuttle hypothesis” and indicate that AQP-2 is the AVP-regulated water channel of the collecting duct cells. There are two types of regulation of AQP-2 gene expression by AVP, namely a prompt alteration in AQP-2 as described above, and a sustained expression of AQP-2.

Water-electrolyte metabolism abnormality : an advance of diagnosis and medical treatment.Water metabolism abnormality.

体内の水分恒常姓の維持はADHの分泌調節と作用発現および口渇感の発生が中心にあるが,これと共にアルドステロンと心房性ナトリウム利尿ホルモンで規定されるナトリウム排泄も水の排泄を規定する重要な調節函子である.水代謝異常は,水出納の異常の結果もたらされた脱水と溢水があり,また水分布の異常として浮腫があるが,経過中または現症における多尿の有無が,治療法選択につながる病態解析の起点となる.