{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T16:41:13Z","timestamp":1785516073657,"version":"3.56.0"},"reference-count":42,"publisher":"National Academy of Sciences","issue":"37","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,9,11]]},"abstract":"<jats:p>\n                    The distal convoluted tubule (DCT) plays an essential role in the reabsorption of NaCl by the kidney, a process that can be inhibited by thiazide diuretics. Parvalbumin (PV), a Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -binding protein that plays a role in muscle fibers and neurons, is selectively expressed in the DCT, where its role remains unknown. We therefore investigated the renal phenotype of PV knockout mice (\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) vs. wild-type (\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>+\/+<\/jats:sup>\n                    ) littermates. PV colocalized with the thiazide-sensitive Na\n                    <jats:sup>+<\/jats:sup>\n                    -Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    cotransporter (NCC) in the early DCT. The\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed increased diuresis and kaliuresis at baseline with higher aldosterone levels and lower lithium clearance. Acute furosemide administration increased diuresis and natriuresis\/kaliuresis, but, surprisingly, did not increase calciuria in\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. NaCl supplementation of\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice increased calciuria at baseline and after furosemide. The\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed no significant diuretic response to hydrochlorothiazide, but an accentuated hypocalciuria. A decreased expression of NCC was detected in the early DCT of\n                    <jats:italic>Pvalb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    kidneys in the absence of ultrastructural and apoptotic changes. The PV-deficient mice had a positive Ca\n                    <jats:sup>2+<\/jats:sup>\n                    balance and increased bone mineral density. Studies in mouse DCT cells showed that endogenous NCC expression is Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -dependent and can be modulated by the levels of PV expression. These results suggest that PV regulates the expression of NCC by modulating intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signaling in response to ATP in DCT cells. They also provide insights into the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -sparing action of thiazides and the pathophysiology of distal tubulopathies.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0702810104","type":"journal-article","created":{"date-parts":[[2007,9,5]],"date-time":"2007-09-05T21:39:58Z","timestamp":1189028398000},"page":"14849-14854","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":89,"title":["Renal expression of parvalbumin is critical for NaCl handling and response to diuretics"],"prefix":"10.1073","volume":"104","author":[{"given":"Hendrica","family":"Belge","sequence":"first","affiliation":[{"name":"Departments of *Nephrology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe","family":"Gailly","sequence":"additional","affiliation":[{"name":"Physiology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beat","family":"Schwaller","sequence":"additional","affiliation":[{"name":"Unit of Anatomy, University of Fribourg, CH-1700 Fribourg, Switzerland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Loffing","sequence":"additional","affiliation":[{"name":"Unit of Anatomy, University of Fribourg, CH-1700 Fribourg, Switzerland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huguette","family":"Debaix","sequence":"additional","affiliation":[{"name":"Departments of *Nephrology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Riveira-Munoz","sequence":"additional","affiliation":[{"name":"Departments of *Nephrology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renaud","family":"Beauwens","sequence":"additional","affiliation":[{"name":"Laboratory of Cell and Molecular Physiology, Universit\u00e9 Libre de Bruxelles Medical School, B-1070 Brussels, Belgium; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Pierre","family":"Devogelaer","sequence":"additional","affiliation":[{"name":"Rheumatology, Universit\u00e9 Catholique de Louvain Medical School, B-1200 Brussels, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joost G.","family":"Hoenderop","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen, 6500 HC Nijmegen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ren\u00e9 J.","family":"Bindels","sequence":"additional","affiliation":[{"name":"Department of Physiology, Radboud University Nijmegen, 6500 HC Nijmegen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Devuyst","sequence":"additional","affiliation":[{"name":"Departments of 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