{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T05:02:47Z","timestamp":1778648567622,"version":"3.51.4"},"reference-count":53,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T00:00:00Z","timestamp":1410825600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Novartis Animal Health"},{"name":"Jane Lewis Seaks Endowment"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vet Pharm & Therapeutics"],"published-print":{"date-parts":[[2015,2]]},"abstract":"Pilot studies in our laboratory revealed that furosemide\u2010induced renin\u2010angiotensin\u2010aldosterone system (RAAS<\/jats:styled-content>) activation was not attenuated by the subsequent co\u2010administration of benazepril. This study was designed to evaluate the effect of benazepril on angiotensin\u2010converting enzyme (ACE<\/jats:styled-content>) activity and furosemide\u2010induced circulatingRAAS<\/jats:styled-content>activation. Our hypothesis was that benazepril suppression ofACE<\/jats:styled-content>activity would not suppress furosemide\u2010induced circulatingRAAS<\/jats:styled-content>activation, indicated by urinary aldosterone concentration. Ten healthy hound dogs were used in this study. The effect of furosemide (2\u00a0mg\/kg p.o., q12h; Group F;n<\/jats:italic>\u00a0=\u00a05) and furosemide plus benazepril (1\u00a0mg\/kg p.o., q24h; GroupFB<\/jats:styled-content>;n<\/jats:italic>\u00a0=\u00a05) on circulatingRAAS<\/jats:styled-content>was determined by plasmaACE<\/jats:styled-content>activity, 4\u20136\u00a0h posttreatment, and urinary aldosterone to creatinine ratio (UA<\/jats:styled-content>ldo:C) on days \u22121, \u22122, 1, 3, and 7. There was a significant increase in the averageUA<\/jats:styled-content>ldo:C (\u03bcg\/g) after the administration of furosemide (Group F baseline [average of days \u22121 and \u22122]UA<\/jats:styled-content>ldo:C\u00a0=\u00a00.41,SD<\/jats:styled-content>0.15; day 1UA<\/jats:styled-content>ldo:C\u00a0=\u00a01.1,SD<\/jats:styled-content>0.56; day 3UA<\/jats:styled-content>ldo:C\u00a0=\u00a00.85,SD<\/jats:styled-content>0.50; day 7UA<\/jats:styled-content>ldo:C\u00a0=\u00a01.1,SD<\/jats:styled-content>0.80,P<\/jats:italic>\u00a0<\u00a00.05). Benazepril suppressedACE<\/jats:styled-content>activity (U\/L) in GroupFB<\/jats:styled-content>(GroupFB<\/jats:styled-content>baselineACE<\/jats:styled-content>\u00a0=\u00a016.4,SD<\/jats:styled-content>4.2; day 1ACE<\/jats:styled-content>\u00a0=\u00a03.5,SD<\/jats:styled-content>1.4; day 3ACE<\/jats:styled-content>\u00a0=\u00a01.6,SD<\/jats:styled-content>1.3; day 7ACE<\/jats:styled-content>\u00a0=\u00a01.4,SD<\/jats:styled-content>1.4,P<\/jats:italic>\u00a0<\u00a00.05) but did not significantly reduce aldosterone excretion (GroupFB<\/jats:styled-content>baselineUA<\/jats:styled-content>ldo:C\u00a0=\u00a00.35,SD<\/jats:styled-content>0.16; day 1UA<\/jats:styled-content>ldo:C\u00a0=\u00a00.79,SD<\/jats:styled-content>0.39; day 3UA<\/jats:styled-content>ldo:C 0.92,SD<\/jats:styled-content>0.48, day 7UA<\/jats:styled-content>ldo:C\u00a0=\u00a00.99,SD<\/jats:styled-content>0.48,P<\/jats:italic>\u00a0<\u00a00.05). Benazepril decreased plasmaACE<\/jats:styled-content>activity but did not prevent furosemide\u2010inducedRAAS<\/jats:styled-content>activation, indicating aldosterone breakthrough (escape). This is particularly noteworthy in that breakthrough is observed at the time of initiation ofRAAS<\/jats:styled-content>suppression, as opposed to developing after months of therapy.<\/jats:p>","DOI":"10.1111\/jvp.12154","type":"journal-article","created":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T06:07:54Z","timestamp":1410847674000},"page":"65-73","source":"Crossref","is-referenced-by-count":27,"title":["Aldosterone breakthrough with benazepril in furosemide\u2010activated renin\u2010angiotensin\u2010aldosterone system in normal dogs"],"prefix":"10.1111","volume":"38","author":[{"given":"A. C.","family":"Lantis","sequence":"first","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. K.","family":"Ames","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. E.","family":"Atkins","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. C.","family":"DeFrancesco","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"B. W.","family":"Keene","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. R.","family":"Werre","sequence":"additional","affiliation":[{"name":"Department of Clinical Sciences College of Veterinary Medicine North Carolina State University Raleigh NC USA"},{"name":"Virginia Maryland Regional College of Veterinary Medicine Blacksburg VA 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