{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T02:01:17Z","timestamp":1787968877135,"version":"build-2784847793"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Heart Failure"],"published-print":{"date-parts":[[2009,11]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background\u2014<\/jats:italic>\n            <\/jats:bold>\n            Urocortin 2 (Ucn2), a novel peptide with therapeutic potential in heart failure, and diuretics have opposing effects on renal function and the renin-angiotensin-aldosterone system. Because any prospective new treatment is likely to be used in conjunction with standard diuretic therapy, it is necessary to investigate the combined effects of these agents.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            Ucn2 and furosemide were administered for 3 hours, both singly and combined, in 7 sheep with pacing-induced heart failure. Compared with time-matched controls, separate Ucn2 and furosemide administration significantly increased urine output (furosemide&gt;Ucn2), urine sodium (furosemide&gt;Ucn2), potassium (furosemide&gt;Ucn2), and creatinine excretion (Ucn2&gt;furosemide) and creatinine clearance (Ucn2&gt;furosemide). Compared with furosemide treatment alone, Ucn2+furosemide produced a further diuresis (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), natriuresis (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), and a sustained increase in creatinine excretion (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) and clearance (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05), without additional potassium elimination. All active treatments reduced mean arterial pressure (Ucn2+furosemide=furosemide&gt;Ucn2), left atrial pressure (Ucn2+furosemide&gt;Ucn2&gt;furosemide), and peripheral resistance (Ucn2+furosemide=Ucn2&gt;furosemide), whereas only Ucn2, singly and in combination with furosemide, increased cardiac output and dP\/dt(max). In contrast to the increase in plasma renin activity elicited by furosemide alone, Ucn2 and Ucn2+furosemide markedly reduced plasma renin activity. All active treatments decreased plasma aldosterone (Ucn2+furosemide=Ucn2&gt;furosemide), whereas only Ucn2 and Ucn2+furosemide reduced vasopressin and natriuretic peptide concentrations.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusion\u2014<\/jats:italic>\n            <\/jats:bold>\n            Ucn2 cotreatment with furosemide enhanced hemodynamic and renal function and diuretic responsiveness (without additional potassium depletion) in experimental heart failure. Furthermore, Ucn2 reversed furosemide-induced increases in plasma renin activity and induced greater decreases in plasma aldosterone and vasopressin. These data indicate that adjunct Ucn2 therapy with diuretics in heart failure is beneficial.\n          <\/jats:p>","DOI":"10.1161\/circheartfailure.109.861336","type":"journal-article","created":{"date-parts":[[2009,9,23]],"date-time":"2009-09-23T00:56:30Z","timestamp":1253667390000},"page":"532-540","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":24,"title":["Urocortin 2 Inhibits Furosemide-Induced Activation of Renin and Enhances Renal Function and Diuretic Responsiveness in Experimental Heart Failure"],"prefix":"10.1161","volume":"2","author":[{"given":"Miriam T.","family":"Rademaker","sequence":"first","affiliation":[{"name":"From the Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch, New Zealand."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Charles","sequence":"additional","affiliation":[{"name":"From the Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch, New Zealand."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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