Parvalbumin: a key protein in early distal tubule NaCl reabsorption.

The cortical distalnephron is committed to the fine regulation of electrolytes and water balance. Several investigations have addressed the molecular mechanisms implicated in this process. The paper by Belge et al. [1] demonstrates the emerging role of parvalbumin (PV) on distal tubule NaCl reabsorption. PV is a divalent cation buffering protein, exclusively expressed in the early distal convoluted tubule (DCT1). The authors show solid data suggesting a functional relationship between PV and the thiazide-sensitive Na+-Cl− cotransporter (NCC), the main entry step for Na+ and Cl− through the apical membrane at this nephron site. PV−/− mice exhibit a salt-losing phenotype characterized by increased diuresis, kaliuresis and high aldosterone levels, a phenotype very similar, although not identical, to the NCC knock-out mice. Accordingly, PV−/− mice manifest decreased expression of NCC, paralleled by no significant diuretic response to hydrochlorothiazide. Furthermore, in vitro studies performed on DCT cells show that PV may regulate NCC expression by modulating the Ca2+-dependent signalling pathway.