Arginine vasopressin regulates CFTR and ClC-2 mRNA expression in rat kidney cortex and medulla

The presence of both CFTR and ClC-2 proteins in the kidney suggest that the y are involved in chloride transport along the nephron but their physiologi cal roles in this organ are not known. To further understand the role of th ese chloride channels we studied Wistar rats subjected to dehydration for 2 days and also the homozygous Brattleboro rats, a strain of Long-Evans rats carrying an autosomal recessive mutation that leads to a deficiency of arg inine-vasopressin (AVP) secretion in the plasma. The expression of CFTR was increased in the medulla of dehydrated Wistar rats and no variation was ob served in the cortex. The expression of both ClC-2 and CFTR mRNAs was low i n the renal cortex and medulla of the homozygous Brattleboro rats but retur ned to normal levels after AVP reposition. By the use of Madine-Darby canin e kidney (MDCK) type I epithelial cells, it was observed that AVP (10(-8). 10(-7) and 10(-6) M) increased CFTR mRNA expression "in vitro" but no effec t was observed when changes in the medium tonicity were caused by the addit ion of sucrose, NaCl, manitol or urea. The modulation of both CFTR and ClC- 2 mRNA by AVR the main hormone involved in the regulation of body fluid osm olality, suggests the participation of these two chloride channels in the r enal tubule transcellular chloride transport modulated by AVP.