{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T13:30:26Z","timestamp":1761744626344},"reference-count":21,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2001,1,1]]},"abstract":" Our study aimed to assess a possible functional role of the Na+<\/jats:sup>\/Ca2+<\/jats:sup> exchanger in the regulation of renal vascular resistance (RVR). Therefore, we investigated the effects of an inhibition of the Na+<\/jats:sup>\/Ca2+<\/jats:sup> exchanger either by lowering the extracellular sodium concentration ([Na+<\/jats:sup>]e<\/jats:sub>) or, pharmacologically on RVR, by using isolated perfused rat kidneys. Graded decreases in [Na+<\/jats:sup>]e<\/jats:sub> led to dose-dependent increases in RVR to 4.3-fold (35 mM Na+<\/jats:sup>). This vasoconstriction was markedly attenuated by lowering the extracellular calcium concentration, by the L-type calcium channel blocker amlodipine or by the chloride channel blocker niflumic acid. Further lowering of [Na+<\/jats:sup>]e<\/jats:sub> to 7 mM led to an increase in RVR to 7.5-fold. In this setting, amlodipine did not influence the magnitude but did influence the velocity of vasoconstriction. Pharmacological blockade of the Na+<\/jats:sup>\/Ca2+<\/jats:sup> exchanger with KB-R7943, benzamil, or nickel resulted in significant vasoconstriction (RVR 2.5-, 1.8-, and 4.2-fold of control, respectively). Our data suggest a functional role of the Na+<\/jats:sup>\/Ca2+<\/jats:sup> exchanger in the renal vascular bed. In conditions of partial replacement of [Na+<\/jats:sup>]e<\/jats:sub>, vasoconstriction is dependent on chloride and L-type calcium channels. A total replacement of [Na+<\/jats:sup>]e<\/jats:sub> leads to a vasoconstriction that is nearly independent of L-type calcium channels. This might be due to an active calcium transport into the cell by the Na+<\/jats:sup>\/Ca2+<\/jats:sup> exchanger. <\/jats:p>","DOI":"10.1152\/ajprenal.2001.280.1.f155","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T13:34:15Z","timestamp":1514036055000},"page":"F155-F161","source":"Crossref","is-referenced-by-count":18,"title":["Functional role of sodium-calcium exchange in the regulation of renal vascular resistance"],"prefix":"10.1152","volume":"280","author":[{"given":"Frank","family":"Schweda","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Physiologie I and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Helga","family":"Seebauer","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie I and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bernhard K.","family":"Kr\u00e4mer","sequence":"additional","affiliation":[{"name":"Klinik und Poliklinik f\u00fcr Innere Medizin II, Universit\u00e4t Regensburg, D-93040 Regensburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Armin","family":"Kurtz","sequence":"additional","affiliation":[{"name":"Institut f\u00fcr Physiologie I and"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.1999.276.1.G293"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1991.261.5.C845"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1038\/337740a0"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.506"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0304-4157(89)90022-1"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.6.C1241"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.4.F598"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.10.4769"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1998.275.2.C423"},{"key":"B10","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.37.22391"},{"key":"B11","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.33.23094"},{"key":"B12","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.3.C628"},{"key":"B13","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.263.3.C635"},{"key":"B14","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1991.tb17284.x"},{"key":"B15","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.510"},{"key":"B16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.276.4.F567"},{"key":"B17","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199909000-00011"},{"key":"B18","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.157.4.9704106"},{"key":"B19","doi-asserted-by":"publisher","DOI":"10.1007\/BF00374822"},{"key":"B20","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1989.256.1.C147"},{"key":"B21","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1994.266.3.C794"}],"container-title":["American Journal of Physiology-Renal Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.2001.280.1.F155","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T20:51:14Z","timestamp":1567975874000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.2001.280.1.F155"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2001,1,1]]},"references-count":21,"journal-issue":{"issue":"1","published-print":{"date-parts":[[2001,1,1]]}},"alternative-id":["10.1152\/ajprenal.2001.280.1.F155"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.2001.280.1.f155","relation":{},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"subject":[],"published":{"date-parts":[[2001,1,1]]}}}