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Effects of chronic administration of urotensin II on cardiac function in rats subjected to volume overload
Author(s) -
Harris Gregory Stuart,
Lust Robert M,
Katwa Laxmansa C
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1197-b
Subject(s) - urotensin ii , medicine , heart failure , cardiac function curve , volume overload , pressure overload , cardiology , endocrinology , mean arterial pressure , blood pressure , heart rate , cardiac hypertrophy , receptor
Urotensin II (UTII) has been implicated in the progression of various cardiovascular diseases, including congestive heart failure, but the effects of chronic UTII administration on cardiac function remain undefined and may be different in normal versus diseased conditions. This study tested the hypothesis that 4 week administration of UTII would exacerbate cardiac dysfunction in volume overloaded (VO) rats. VO was created by formation of an aortocaval AV fistula in Sprague‐Dawley rats (n=8). Animals were separated into control, UTII (osmotic mini pumps) only, VO, and UTII+ VO (n=4 per group). After 4 weeks left ventricular function was assessed in all groups. Mean arterial pressure was not changed in the UTII and UTII+VO groups compared to controls, while significantly reduced in the VO group. Left ventricular peak systolic pressure (LVPSP) was significantly decreased in the UTII and VO groups compared to controls, while UTII+VO resulted in pressures not significantly different from control. Finally, both positive and negative dP/dt also were decreased significantly in both UTII and VO groups, while the UTII+VO exhibited a trend toward significance compared to VO alone. These data demonstrate that UTII decreases cardiac function in normal animals, while apparently improving function in the presence of VO. Further studies will be needed to determine the exact role of UTII in the progression of congestive heart failure, and the mechanisms of its effects in normal myocardium.