{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:54:28Z","timestamp":1790873668115,"version":"4.1.0"},"reference-count":90,"publisher":"The Company of Biologists","issue":"9","license":[{"start":{"date-parts":[[1998,5,1]],"date-time":"1998-05-01T00:00:00Z","timestamp":893980800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/www.biologists.com\/user-licence-1-1\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[1998,5,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:p>Regulatory volume decrease (RVD) following hypo-osmotic stimulation was studied using videometric methods in isolated proximal renal tubules from trout (Salmo trutta). The relative tubule diameter increased by 132.0\u00b14.8 % (maximum swelling within 1 min at 15 and 25 \u00b0C and within 4 min at 10 \u00b0C) following a change from iso-osmotic (290 mosmol kg\u22121) to hypo-osmotic (160 mosmol kg\u22121) Ringer\u2019s solution. The tubule diameter subsequently decreased to approximately one-quarter of the maximal value. Ouabain (1 mmol l\u22121) reduced cell swelling and inhibited the RVD response by 28.0\u00b110.5 %. Furthermore, increasing the bath K+ concentration by 30 mmol l\u22121 inhibited RVD by 76.5\u00b13.6 %. The K+ channel blocker quinine, but not Ba2+ (1 and 2 mmol l\u22121), significantly decreased the RVD response (by 25.0\u00b15.4 and 72.3\u00b15.1 % at 0.1 and 0.5 mmol l\u22121, respectively). Similarly, increasing the Cl\u2212 concentration in the bath from 47 to 102 mmol l\u22121 induced a significant reduction (45.2\u00b17.9 %) in RVD. The RVD response was also markedly reduced (by 54.7\u00b15.3 %) by the Cl\u2212 channel blocker indacrinone (MK-196; 0.5 mmol l\u22121), but only marginally by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 1, 5, 8 and 10 \u00b5mol l\u22121). Addition of the K+\/Cl\u2212 symport inhibitor furosemide (0.1 mmol l\u22121) resulted in a 39.8\u00b13.9 % inhibition of RVD. This inhibition could be completely overcome by simultaneous administration of 1 \u00b5mol l\u22121 tributyltin (anion exchanger) and furosemide.<\/jats:p>\n               <jats:p>Chelation of either extracellular (1 mmol l\u22121 EGTA) or both extra- and intracellular Ca2+ (1 mmol l\u22121 EGTA, 10 \u00b5mol l\u22121 A23187) had no effect on this RVD process. Furthermore, as measured using the fluorescent dye Fura-2\/AM, there was no increase in the intracellular free Ca2+ concentration upon hypo-osmotic stimulation. Administration of the 5-lipoxygenase antagonist ETH 615-139 (20 \u00b5mol l\u22121), however, induced a 60 % inhibition of RVD. Simultaneous addition of ETH-615 and either the K+ ionophore gramicidin (0.5 mmol l\u22121) or the anion exchanger tributyltin (1 \u00b5mol l\u22121) could not reverse the ETH 615-139 inhibition. Finally, administration of the cycloxygenase inhibitor indomethacin had only a small, but significant, effect on RVD.<\/jats:p>\n               <jats:p>We conclude that RVD following hypo-osmotic swelling is in these cells a temperature- and ouabain-sensitive process that appears to be the result of K+ efflux through quinine-sensitive, Ba2+-insensitive K+ channels and Cl\u2212 efflux through an MK-196- and furosemide-sensitive Cl\u2212 conductance that is relatively unaffected by NPPB. This KCl efflux seems to be regulated by eicosanoids produced by the 5-lipoxygenase. Arachidonic acid metabolites from the cycloxygenase pathway are not involved in this process. Similarly, neither extra-nor intracellular Ca2+ appears to be important for the signalling of RVD.<\/jats:p>","DOI":"10.1242\/jeb.201.9.1405","type":"journal-article","created":{"date-parts":[[2021,4,25]],"date-time":"2021-04-25T05:27:20Z","timestamp":1619328440000},"page":"1405-1419","source":"Crossref","is-referenced-by-count":23,"title":["Cell Volume Regulation In Proximal Renal Tubules From Trout (<i>Salmo Trutta<\/i>)"],"prefix":"10.1242","volume":"201","author":[{"given":"Hilde","family":"Kanli","sequence":"first","affiliation":[{"name":"Division of General Physiology, University of Oslo, Norway Department of Biology ,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eli","family":"Norderhus","sequence":"additional","affiliation":[{"name":"Division of General Physiology, University of Oslo, Norway Department of Biology ,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[1998,5,1]]},"reference":[{"key":"2024032020413526000_JEXBIO_201_9_1405C1","first-page":"F1093","article-title":"Luminal prostaglandin E2 modulates sodium and water transport in rabbit cortical collecting ducts","volume":"268","author":"Ando","year":"1995","journal-title":"Am. 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