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Urocortin 2 acutely decreases myocardial stiffness.

Title
Urocortin 2 acutely decreases myocardial stiffness.
Type
Summary of Presentation in an International Conference
Year
2007
Authors
Brás-Silva C
(Author)
FMUP
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Duarte AJ
(Author)
Other
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Monteiro-Sousa D
(Author)
Other
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Leite-Moreira AF
(Author)
FMUP
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Conference proceedings International
Pages: 39-40
Heart Failure 2007
Hamburgo, Alemanha, 09 a 12 de Junho de 2007
Scientific classification
FOS: Medical and Health sciences > Other medical sciences
Other information
Resumo (PT): Background: The urocortin (Ucn) peptides Ucn1, Ucn2, and Ucn3 are recently isolated members of the corticotropin-releasing factor (CRF) family. Urocortin II enhances contractility via CRF2 receptor-mediated stimulation of protein kinase A. As protein kinase A is a well known modulator of diastolic function, in the current study, we investigated the, yet unknown, acute effects of Ucn2 on the diastolic properties of the myocardium. Methods: Effects of increasing concentrations of Ucn2 (10-8 to 10-6M) were evaluated in isolated right papillary muscles (n=12) from male New Zealand White rabbits (Krebs-Ringer: 1,8mM CaCl2, 35°C). Reported parameters include: active tension (AT; mN/mm2), maximum velocities of tension rise and tension decline (dT/dtmax e dT/dtmin, respectively; mN/mm2/s), passive tension (PT; mN/mm2) and muscle length (L; L/Lmax). Only significant results (mean±SEM, p<0.05) are given, expressed as % change from baseline. Results: Ucn2 increased 68.4±7.5% AT, 187.5±13.5% dT/dtmax and 140.3±13.8% dT/dtmin in the concentration range of this study. It also promoted a concentration-dependent increase in resting muscle length up to 1.012±0.004 L/Lmax at the highest concentration. Correcting muscle length to its initial value resulted in a 29.6±8.9% decrease of PT, indicating a decrease in muscle stiffness. Conclusion: The present study demonstrated a novel effect of Ucn2 on the diastolic properties of the myocardium, which consisted on a concentration dependent acute decrease of myocardial stiffness. This effect is a potentially powerful physiologic mechanism, as it may allow the heart to reach the same diastolic volume with up to 30% lower filling pressures. These results support a role for Ucn2 in the pathophysiology of heart failure and points out to its therapeutic potential in this disease.
Language: English
Type (Professor's evaluation): Scientific
Notes: Heart Failure 2007, published in journal, European Journal of Heart Failure Supplements 2007; 6 (Suppl 1): 39-40.
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