Vasopressin and Aquaporin-2 Water Channel in Impaired Water Excretion

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In the present study we demonstrated the roles of arginine vasopressin (AVP) and aquaporin-2 (AQP2) water channel in impaired water excretion. In the in vitro study the AQP2 promoter assay clarified the presence of tonicity-response element (TonE) in the AQP2 5'-flanking region (-570～-560 bp) as well as cAMP-response element (CRE) for activating AQP2 transcription. An exposure of cells to hypotonic solution diminished the cAMP-activated AQP2 promoter activity. In the in vivo study the expression of AQP2 mRNA and protein were increased in concert with an increase in plasma AVP in the glucocorticoid-deficient rats. The phenomenon was much manifest in the elder rats with glucocorticoid deficiency. The enhanced expressions of AQP2 mRNA and protein were normalized in the rats after glucocorticoid replacement. Varying levels of serum Na were found in the patients with acute infectious diseases. The group of hyponatremia had an elevation of plasma AVP despite of no reduction in circulatory blood volume. The elevated plasma IL-1β could centrally stimulate AVP release, and produce impaired water excretion and hyponatremia. There was 20.9% of the patients with acute myocardial infarction having hyponatremia within 72 hours after the onset. Plasma AVP was significantly increased in the hyponatremic patients compared with that in the normonatremic ones. There was poor short- and long-term prognosis in the patients with hyponatremia.