{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T22:53:29Z","timestamp":1770072809121,"version":"3.49.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"23","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2005,12,6]]},"abstract":"\n \n Background\u2014<\/jats:italic>\n <\/jats:bold>\n Urocortin 2 (Ucn2) has potent cardiovascular actions and may participate in the pathophysiology of heart failure (HF). The integrated hemodynamic, endocrine, and renal effects of Ucn2 are unknown.\n <\/jats:p>\n \n \n Methods and Results\u2014<\/jats:italic>\n <\/jats:bold>\n Eight sheep received incremental intravenous boluses of murine Ucn2 (10, 50, and 100 \u03bcg at 2-hour intervals) before (normal) and during pacing-induced HF. Compared with control data, Ucn2 induced rapid and dose-dependent increases in cardiac output (peak effects: normal 4.3\u00b10.2 versus 6.1\u00b10.2 L\/min,\n P<\/jats:italic>\n <0.001; HF 2.3\u00b10.1 versus 4.5\u00b10.2 L\/min,\n P<\/jats:italic>\n <0.001) and reductions in peripheral resistance (normal 20.2\u00b11.0 versus 15.2\u00b10.8 mm Hg\/L per minute,\n P<\/jats:italic>\n <0.01; HF 32.2\u00b11.7 versus 13.6\u00b10.5 mm Hg\/L per minute,\n P<\/jats:italic>\n <0.001) and left atrial pressure (normal 4.3\u00b10.3 versus 0.5\u00b10.2 mm Hg,\n P<\/jats:italic>\n <0.01; HF 22.9\u00b10.6 versus 5.1\u00b11.8 mm Hg,\n P<\/jats:italic>\n <0.001). Mean arterial pressure was minimally elevated in normals and decreased in HF (both\n P<\/jats:italic>\n <0.01). In both states, Ucn2 reduced plasma atrial natriuretic peptide levels (normal 13\u00b12 versus 10\u00b12 pmol\/L; HF 200\u00b120 versus 72\u00b110 pmol\/L) and similarly increased corticotropin, cortisol, and Ucn1 (all\n P<\/jats:italic>\n <0.001). In HF only, Ucn2 dose dependently decreased plasma vasopressin (3.09\u00b10.36 versus 1.62\u00b10.12 pmol\/L,\n P<\/jats:italic>\n <0.01), renin (2.98\u00b11.17 versus 0.69\u00b10.10 nmol\/L per hour,\n P<\/jats:italic>\n <0.001), aldosterone (1186\u00b1303 versus 364\u00b1122 pmol\/L,\n P<\/jats:italic>\n <0.001), endothelin-1 (3.39\u00b10.23 versus 2.56\u00b10.18 pmol\/L,\n P<\/jats:italic>\n <0.01), epinephrine (1633\u00b1260 versus 657\u00b1142 pmol\/L,\n P<\/jats:italic>\n <0.01), and brain natriuretic peptide (36\u00b13 versus 18\u00b14 pmol\/L,\n P<\/jats:italic>\n <0.001) concentrations. Renal effects, including increased urine volume (1.7-fold,\n P<\/jats:italic>\n <0.05), sodium excretion (>12-fold,\n P<\/jats:italic>\n <0.01), and creatinine excretion (1.3-fold,\n P<\/jats:italic>\n <0.001), also occurred only in HF.\n <\/jats:p>\n \n \n Conclusions\u2014<\/jats:italic>\n <\/jats:bold>\n Ucn2 has marked and beneficial hemodynamic, hormonal, and renal effects in experimental HF. These results support a role for Ucn2 in pressure\/volume homeostasis in HF and suggest that the peptide may have therapeutic potential in this disease.\n <\/jats:p>","DOI":"10.1161\/circulationaha.105.561308","type":"journal-article","created":{"date-parts":[[2005,12,5]],"date-time":"2005-12-05T21:48:14Z","timestamp":1133819294000},"page":"3624-3632","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":78,"title":["Integrated Hemodynamic, Hormonal, and Renal Actions of Urocortin 2 in Normal and Paced Sheep"],"prefix":"10.1161","volume":"112","author":[{"given":"Miriam T.","family":"Rademaker","sequence":"first","affiliation":[{"name":"From Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch, New Zealand."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Vicky A.","family":"Cameron","sequence":"additional","affiliation":[{"name":"From Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch, New Zealand."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher J.","family":"Charles","sequence":"additional","affiliation":[{"name":"From Christchurch Cardioendocrine Research Group, Christchurch School of Medicine, Christchurch, New Zealand."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. 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