Resumo (PT):
Acute effects of angiotensin II (AT-II) on the diastolic properties of the myocardium
were only recently described. AT-II acutely increased myocardial distensibility
through AT-1 receptor stimulation. In the present study we evaluated its effects
on myocardial stiffness with passive length-tension relations and tried to clarify
some of the underlying mechanisms.
Increasing doses of AT-II (10e-9 to 10e-5 M) were added to rabbit right papillary
muscles immersed in a modified Krebs solution (0.6 Hz, 1.8 mM Ca2+, 35°C)
at baseline (n=11) and in presence of chelerythrine, a protein kinase C (pKC)
inhibitor (CHE, 10e-5M; n=8), or 5-(N-methyl-N-isobutyl)-amiloride, an inhibitor of
Na+/H+ exchanger (MIA; 10e-6 M; n=10). Calculated parameters: resting tension
(RT), active tension (AT), peak rate of tension rise (dT/dtmax), resting length (RL)
and peak shortening (PS). Results presented as mean±SEM in % of baseline
(p<0.05).
At baseline, AT-II induced a dose dependent positive inotropic effect and increased
RL. At 10e-5 M, AT-II increased 43.3±6.25% AT, 58.6±9.6% dT/dtmax,
35.8±4.4% PS and 1.96±0.4% RL. Restoring RL to the value it presented before
addition of AT-II resulted in a decrease in RT of 46±4%. In addition, AT-II right and
downward shifted the passive length-tension relation (Figure). Effects of AT-II on
RT were attenuated by MIA (23±5%) and almost blunted by CHE (11±4%).
Passive length-tension relation
In conclusion, AT-II significantly decreased RT and rightward shifted the passive
length-tension relation, indicating a decrease in myocardial stiffness, an effect
that was mediated by pKC and Na+/H+ exchanger. These results indicate that
AT-II acutely modulates diastolic function and therefore may be involved in the
response to acute changes in ventricular filling dynamics.
Language:
English
Type (Professor's evaluation):
Scientific
Notes:
27th Congress of the European-Society-of-Cardiology, published in journal, European Heart Journal. 2005; Vol.26 (Abstract P535)(Suppl1):64-64.