Angiotensin II acutely increases ventricular distensibility.

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

Authors

Guerra MS (Author) FMUP; Castro-Chaves P (Author) FMUP; Brás-Silva C (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Journal of Heart Failure

Initial page: 83

ESC Annual Congress 2006

Helsínquia, Finlândia, 17 a 20 de Junho de 2006

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

CORDIS: Health sciences > Medical sciences > Medicine > Cardiology

Other information

Resumo (PT): Angiotensin II (AngII) has a central role in cardiovascular homeostasis, acutely as a vasoconstrictor and a positive inotropic agent and chronicaJly promoting mitogenesis, growth and extracellular matrix synthesis, thereby contributing to ventricular remodelling, cardiac hypertrophy and to the deterioration of systolic and diastolic functions. Recently we showed that AngII increases myocardial distensibility of isolated cardiac muscles. Our objective was to test if this effect is also observed in the in situ intact heart. The study was performed in 6 anesthetized open-chest rabbits (2.0"1,0.2 kg) instrumented with a left ventricular (LV) high-fidelity micromanometer to measure intracavitary pressures. After stabilization and baseline measurements a silk suture was placed around the ascending aorta to performing an aortic banding, in order to get an increase of ~50% of LV pressure during 30'. After that aortic banding was released and AngII infusion (10l~g/kg/min) was started to get a similar LV pressure. We observed that AngII progressively increased systolic LV pressure from 74"1,2 to lll-t-4mmHg and decreased end-diastolic and minimum LV pressures from 7.1"1,0.7 to 5.94-0.5mmHg and 6.0-1,0.3 to 4.6-t-0.6mmHg, respectively (p<0.05). Although aortic banding promoted a similar increase of systolic LV pressure from 74-1,2 to ll2-t-4mmHg it elevated end-diastolic (from 7.1-1,0.3 to 10.04-0.3mmHg) and minimum (from 6.0-1,0.3 to 8.44-0.5mmHg) LV pressures (p<0.05). This study provides strong evidence that AngII induces a significant decrease of diastolic LV pressures, which averages ~40% when its effect is assessed at similar systolic pressures. The effect of AngII on myocardial distensibility, previously described in vitro, was, therefore, also observed in vivo. This novel effect of AngII which may improve ventricular filling expands our concepts regarding the acute neurohumoraJ modulation of diastolic function.

Language: English

Type (Professor's evaluation): Scientific

Notes: ESC Annual Congress 2006, published in journal, European Journal of Heart Failure. 2006; Vol.5(Suppl.1):83-83.