title: Aldosterone and high-NaCl diet modulate ClC-2 chloride channel gene expression in rat kidney.
abstract: It is well known that Na+ reabsorption in the kidney can be regulated by aldosterone. Although Cl- is the most abundant anion present in the extra cellular fluids the involvement of aldosterone in the regulation of Cl- conductance through Cl- channels at the molecular level is unknown. In this study, the effects of aldosterone and high-Na+ diet on the expression of ClC-2, a cell volume-, pH- and voltage-sensitive Cl- channel, was examined in the rat kidney. Total RNA isolated from Wistar rats fed a high-Na+ diet for 5 days, furosemide treatment, adrenalectomy and adrenalectomy with replacement of normal plasma levels of aldosterone were compared by the use of ribonuclease protection assay (RPA), and/or a semi-quantitative RT-PCR. The high-Na+ diet reduced renal mRNA and protein ClC-2 expression. The renal expression of ClC-2 mRNA decreased in adrenalectomized rats and was restored by plasma aldosterone replacement. In addition, the semi-quantitative RT-PCR in different segments of the nephron showed that these changes were secondary to the modulation of ClC-2 mRNA expression by aldosterone in the cortical and medullary segments of thick ascending limbs of Henle's loop. These results suggest that ClC-2 may be involved with aldosterone-induced Cl- transport in the kidney.
authors.affiliation: Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS-Bloco G, CEP 21949-900 Rio de Janeiro, Brazil.
authors.forename: Débora S
authors.initials: DS
authors.lastname: Ornellas
authors.forename: Danielle S
authors.initials: DS
authors.lastname: Nascimento
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Christoph
authors.forename: William B
authors.initials: WB
authors.lastname: Guggino
authors.forename: Marcelo M
authors.initials: MM
authors.lastname: Morales
mesh_terms: D000315:Adrenalectomy; D000450:Aldosterone / Q000494:pharmacology*; D000818:Animals; D015139:Blotting, Southern; D015153:Blotting, Western; D018118:Chloride Channels / Q000096:biosynthesis* / Q000235:genetics*; D004232:Diuretics / Q000494:pharmacology; D004573:Electrolytes / Q000378:metabolism; D005665:Furosemide / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009399:Nephrons / Q000187:drug effects / Q000378:metabolism; D023282:Nuclease Protection Assays; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*
chemical_list: D018118:Chloride Channels; D004232:Diuretics; D004573:Electrolytes; D017673:Sodium Chloride, Dietary; D000450:Aldosterone; D012313:RNA; D005665:Furosemide