{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,2]],"date-time":"2026-01-02T17:15:19Z","timestamp":1767374119058,"version":"3.37.3"},"reference-count":42,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL-028982"],"award-info":[{"award-number":["HL-028982"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2017,12,1]]},"abstract":"<jats:p> Afferent arteriole (Af-Art) resistance is modulated by two intrinsic nephron feedbacks: 1) the vasoconstrictor tubuloglomerular feedback (TGF) mediated by Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>-2Cl<jats:sup>\u2212<\/jats:sup> cotransporters (NKCC2) in the macula densa and blocked by furosemide and 2) the vasodilator connecting tubule glomerular feedback (CTGF), mediated by epithelial Na<jats:sup>+<\/jats:sup> channels (ENaC) in the connecting tubule and blocked by benzamil. High salt intake reduces Af-Art vasoconstrictor ability in Dahl salt-sensitive rats (Dahl SS). Previously, we measured CTGF indirectly, by differences between TGF responses with and without CTGF inhibition. We recently developed a new method to measure CTGF more directly by simultaneously inhibiting NKCC2 and the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup> exchanger (NHE). We hypothesize that in vivo during simultaneous inhibition of NKCC2 and NHE, CTGF causes an Af-Art dilatation revealed by an increase in stop-flow pressure (P<jats:sub>SF<\/jats:sub>) in Dahl SS and that is enhanced with a high salt intake. In the presence of furosemide alone, increasing nephron perfusion did not change the P<jats:sub>SF<\/jats:sub> in either Dahl salt-resistant rats (Dahl SR) or Dahl SS. When furosemide and an NHE inhibitor, dimethylamiloride, were perfused simultaneously, an increase in tubular flow caused Af-Art dilatation that was demonstrated by an increase in P<jats:sub>SF.<\/jats:sub> This increase was greater in Dahl SS [4.5\u2009\u00b1\u20090.4 (SE) mmHg] than in Dahl SR (2.5\u2009\u00b1\u20090.3 mmHg; P &lt; 0.01). We confirmed that CTGF causes this vasodilation, since benzamil completely blocked this effect. However, a high salt intake did not augment the Af-Art dilatation. We conclude that during simultaneous inhibition of NKCC2 and NHE in the nephron, CTGF induces Af-Art dilatation and a high salt intake failed to enhance this effect. <\/jats:p>","DOI":"10.1152\/ajprenal.00320.2017","type":"journal-article","created":{"date-parts":[[2017,8,23]],"date-time":"2017-08-23T20:10:32Z","timestamp":1503519032000},"page":"F1209-F1215","source":"Crossref","is-referenced-by-count":4,"title":["Effect of salt intake on afferent arteriolar dilatation: role of connecting tubule glomerular feedback (CTGF)"],"prefix":"10.1152","volume":"313","author":[{"given":"Hong","family":"Wang","sequence":"first","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8445-9665","authenticated-orcid":false,"given":"Cesar A.","family":"Romero","sequence":"additional","affiliation":[{"name":"Hypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. 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