{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T14:19:05Z","timestamp":1784989145698,"version":"3.55.0"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2015,7,1]],"date-time":"2015-07-01T00:00:00Z","timestamp":1435708800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Internal Grant Agency of the Ministry of Health the Czech Republic","award":["NT\/14012-3\/2013"],"award-info":[{"award-number":["NT\/14012-3\/2013"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The detailed mechanisms determining the course of congestive heart failure (<jats:styled-content style=\"fixed-case\">CHF<\/jats:styled-content>) in hypertensive subjects with associated renal dysfunction remain unclear. In Ren\u20102 transgenic rats (<jats:styled-content style=\"fixed-case\">TGR<\/jats:styled-content>), a model of angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">ANG II<\/jats:styled-content>)\u2010dependent hypertension, <jats:styled-content style=\"fixed-case\">CHF<\/jats:styled-content> was induced by volume overload achieved by creation of the aorto\u2010caval fistula (<jats:styled-content style=\"fixed-case\">ACF<\/jats:styled-content>). In these rats we investigated the putative pathophysiological contribution of epoxyeicosatrienoic acids (<jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>s) and compared it with the role of the renin\u2010angiotensin system (<jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>). We found that untreated <jats:styled-content style=\"fixed-case\">ACF TGR<\/jats:styled-content> exhibited marked intrarenal and myocardial deficiency of <jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>s and impairment of renal function. Chronic treatment of these rats with <jats:italic>cis<\/jats:italic>\u20104\u2010[4\u2010(3\u2010adamantan\u20101\u2010yl\u2010ureido)cyclohexyloxy]benzoic acid (<jats:italic>c\u2010<\/jats:italic><jats:styled-content style=\"fixed-case\">AUCB<\/jats:styled-content>, 3\u00a0mg\/L in drinking water), an inhibitor of soluble epoxide hydrolase (s<jats:styled-content style=\"fixed-case\">EH<\/jats:styled-content>) which normally degrades <jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>s, increased intrarenal and myocardial <jats:styled-content style=\"fixed-case\">EET<\/jats:styled-content>s, markedly improved survival rate, and increased renal blood flow, glomerular filtration rate and fractional sodium excretion, without altering <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content> activity. Chronic angiotensin\u2010converting enzyme inhibition (<jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i) with trandolapril, (6\u00a0mg\/L in drinking water) improved survival rate even more, and also inhibited the development of renal dysfunction; these beneficial actions were associated with significant suppression of the vasoconstrictor\/sodium retaining axis and further activation of the vasodilatory\/natriuretic axis of the systemic and intrarenal <jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>, without modifying tissue availability of biologically active fatty acid epoxides. In conclusion, these findings strongly suggest that chronic s<jats:styled-content style=\"fixed-case\">EH<\/jats:styled-content> inhibition and chronic treatment with <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i, each of them altering a different vasoactive system, delay or even prevent the onset of decompensation of <jats:styled-content style=\"fixed-case\">CHF<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">ACF TGR<\/jats:styled-content>, probably by preventing the development of renal dysfunction.<\/jats:p>","DOI":"10.1111\/1440-1681.12419","type":"journal-article","created":{"date-parts":[[2015,5,13]],"date-time":"2015-05-13T07:59:07Z","timestamp":1431503947000},"page":"795-807","source":"Crossref","is-referenced-by-count":42,"title":["Inhibition of soluble epoxide hydrolase counteracts the development of renal dysfunction and progression of congestive heart failure in <scp>R<\/scp>en\u20102 transgenic hypertensive rats with aorto\u2010caval fistula"],"prefix":"10.1111","volume":"42","author":[{"given":"Lud\u011bk","family":"\u010cervenka","sequence":"first","affiliation":[{"name":"Centre for Experimental Medicine Institute for Clinical and Experimental Medicine Prague Czech Republic"},{"name":"Department of Pathophysiology 2nd Faculty of Medicine Charles University Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vojt\u011bch","family":"Melenovsk\u00fd","sequence":"additional","affiliation":[{"name":"Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zuzana","family":"Huskov\u00e1","sequence":"additional","affiliation":[{"name":"Centre for Experimental Medicine Institute for Clinical and Experimental Medicine Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"\u0160karoupkov\u00e1","sequence":"additional","affiliation":[{"name":"Centre for Experimental Medicine Institute for Clinical and Experimental Medicine Prague Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akira","family":"Nishiyama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Kagawa University Kagawa Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janusz","family":"Sadowski","sequence":"additional","affiliation":[{"name":"Department of Renal and Body Fluid Physiology M. 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