{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T21:29:20Z","timestamp":1778275760979,"version":"3.51.4"},"reference-count":39,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2002,2,1]]},"abstract":"<jats:p>ANG II is a modulator of tubuloglomerular feedback (TGF); however, the site of its action remains unknown. Macula densa (MD) cells sense changes in luminal NaCl concentration ([NaCl]<jats:sub>L<\/jats:sub>) via a Na-2Cl-K cotransporter, and these cells do possess ANG II receptors. We tested whether ANG II regulates Na-2Cl-K cotransport in MD cells. MD cell Na<jats:sup>+<\/jats:sup>concentration ([Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>) was measured using sodium-binding benzofuran isophthalate with fluorescence microscopy. Resting [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>in MD cells was 27.7 \u00b1 1.05 mM ( n = 138) and increased (\u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>) by 18.5 \u00b1 1.14 mM ( n = 17) at an initial rate (\u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>\/\u0394 t) of 5.54 \u00b1 0.53 \u00d7 10<jats:sup>\u22124<\/jats:sup>U\/s with an increase in [NaCl]<jats:sub>L<\/jats:sub>from 25 to 150 mM. Both \u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>and \u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>\/\u0394 t were inhibited by 80% with 100 \u03bcM luminal furosemide. ANG II (10<jats:sup>\u22129<\/jats:sup>or 10<jats:sup>\u221212<\/jats:sup>M) added to the lumen increased MD resting [Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>and [NaCl]<jats:sub>L<\/jats:sub>-dependent \u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>and caused a twofold increase in \u0394[Na<jats:sup>+<\/jats:sup>]<jats:sub>i<\/jats:sub>\/\u0394 t. Bath (10<jats:sup>\u22129<\/jats:sup>M) ANG II also stimulated cotransport activity, and there was no additive effect of simultaneous addition of ANG II to bath and lumen. The effects of luminal ANG II were furosemide sensitive and abolished by the AT<jats:sub>1<\/jats:sub>receptor blocker candesartan. ANG II at 10<jats:sup>\u22126<\/jats:sup>M failed to stimulate the cotransporter, whereas increased cotransport activity could be restored by blocking AT<jats:sub>2<\/jats:sub>receptors with PD-123,\u2009319. Thus ANG II may modulate TGF responses via alterations in MD Na-2Cl-K cotransport activity.<\/jats:p>","DOI":"10.1152\/ajprenal.00129.2001","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:33:46Z","timestamp":1425414826000},"page":"F301-F306","source":"Crossref","is-referenced-by-count":46,"title":["Angiotensin II directly stimulates macula densa Na-2Cl-K cotransport via apical AT<sub>1<\/sub>receptors"],"prefix":"10.1152","volume":"282","author":[{"given":"Gergely","family":"Kov\u00e1cs","sequence":"first","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Departments of Medicine and Physiology, University of Alabama at Birmingham, Birmingham, Alabama 35294; and"},{"name":"International Nephrology Research and Training Center, Institute of Pathophysiology, Semmelweis University, H-1089 Budapest, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J\u00e1nos","family":"Peti-Peterdi","sequence":"additional","affiliation":[{"name":"Nephrology Research and Training Center, Division of Nephrology, Departments of Medicine and Physiology, University of Alabama at Birmingham, Birmingham, Alabama 35294; and"},{"name":"International Nephrology Research and Training Center, Institute of Pathophysiology, Semmelweis University, H-1089 Budapest, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L\u00e1szl\u00f3","family":"Rosivall","sequence":"additional","affiliation":[{"name":"International Nephrology Research and Training Center, Institute of Pathophysiology, Semmelweis University, H-1089 Budapest, Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. 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