{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T05:26:46Z","timestamp":1790054806798,"version":"4.0.1"},"reference-count":59,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2011,3]]},"abstract":"<jats:p>Collecting duct (CD) endothelin-1 (ET-1) is an important autocrine inhibitor of CD Na<jats:sup>+<\/jats:sup>reabsorption. Salt loading is thought to increase CD ET-1 production; however, definitive evidence of this, as well as understanding of the mechanisms transducing this effect, is lacking. Tubule fluid flow increases in response to Na<jats:sup>+<\/jats:sup>loading; hence, we studied flow modulation of CD ET-1 production. Three days of a high-salt diet increased mouse and rat inner medullary CD (IMCD) ET-1 mRNA expression. Acute furosemide infusion increased urinary ET-1 excretion in anesthetized rats. Primary cultures of mouse or rat IMCD detached in response to flow using a closed perfusion chamber, consequently a CD cell line (mpkCCDcl4) was examined. Flow increased ET-1 mRNA at shear stress rates exceeding 1 dyne\/cm<jats:sup>2<\/jats:sup>, with the maximal effect seen between 2 and 10 dyne\/cm<jats:sup>2<\/jats:sup>. Induction of ET-1 mRNA was first evident after 1 h, and most apparent after 2 h, of flow. Inhibition of calmodulin or dihydropyridine-sensitive Ca<jats:sup>2+<\/jats:sup>channels did not alter the flow response; however, chelation of intracellular Ca<jats:sup>2+<\/jats:sup>or removal of extracellular Ca<jats:sup>2+<\/jats:sup>largely prevented flow-stimulated ET-1 mRNA accumulation. Downregulation of protein kinase C (PKC) using phorbol 12-myristate 13-acetate, or PKC inhibition with calphostin C, markedly reduced flow-stimulated ET-1 mRNA levels. Flow-stimulated ET-1 mRNA accumulation was abolished by inhibition of phospholipase C (PLC). Taken together, these data indicate that flow increases CD ET-1 production and this is dependent on extracellular and intracellular Ca<jats:sup>2+<\/jats:sup>, PKC, and PLC. These studies suggest a novel pathway for coupling alterations in extracellular fluid volume to CD ET-1 production and ultimately control of CD Na<jats:sup>+<\/jats:sup>reabsorption.<\/jats:p>","DOI":"10.1152\/ajprenal.00530.2010","type":"journal-article","created":{"date-parts":[[2010,12,23]],"date-time":"2010-12-23T02:56:43Z","timestamp":1293073003000},"page":"F650-F656","source":"Crossref","is-referenced-by-count":44,"title":["Flow regulation of collecting duct endothelin-1 production"],"prefix":"10.1152","volume":"300","author":[{"given":"Brianna","family":"Lyon-Roberts","sequence":"first","affiliation":[{"name":"Division of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin A.","family":"Strait","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah; 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