The novel role of urotensin II on the diastolic properties of myocardium.

• Type: Summary of Presentation in an International Conference
• Date: 2006

Authors

Fontes-Sousa AP (Author) Other; Brás-Silva C (Author) FMUP; Monteiro-Sousa D (Author) Other; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Heart Journal

Initial page: 846

World Congress of Cardiology

Barcelona, SPAIN, 02 a 06 de Setembro de 2006

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Background: Urotensin II (U-II) is a peptide expressed, together with its receptor, in the central nervous system and in many peripheral tissues, including the cardiovascular system. In the latter, U-II has been shown to modulate the vascular tonus, myocardial contraction, heart rate and cardiac fibrosis and hypertrophy. In the current study, we investigated the, yet unknown, acute effects of U-II on the diastolic properties of the myocardium. Methods: Effects of increasing concentrations of U-II (10-8 to 10-6M) were evaluated in isolated right papillary muscles (n=13) 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), resting tension (RT; mN/mm2) and muscle length (L; L/Lmax). Only significant results (means±SEM, p<0.05) are given, expressed as % change from baseline. Results: U-II had no significant effects on AT, dT/dtmax and dT/dtmin in the concentration range of this study. It, however, promoted a concentration-dependent increase in resting muscle length up to 1.007±0.0016 L/Lmax at the highest concentration. Correcting muscle length to its initial value resulted in a 20.6±3.59% decrease of RT, indicating decreased muscle stiffness. Conclusion: The present study demonstrated a novel effect of U-II 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 20% lower filling pressures. Furthermore, as the plasmatic levels of U-II are increased in heart failure, these results might help to better understand the physiopathology of this syndrome.

Language: English

Type (Professor's evaluation): Scientific

Notes: XVth World Congress of Cardiology, published in journal, European Heart Journal. 2006; Vol.27(Suppl.1):846-846.