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Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah 84112-5000
In this study we examined
Na+/H+
exchange activity, Ca2+
transients, and contractility in rabbit ventricular myocytes isolated from normal and chronically (8-12 wk) infarcted left ventricles. Myocytes from infarcted hearts (post-MI myocytes) were isolated from
the peri-infarcted region of the left ventricle. Intracellular pH
(pHi) and
Ca2+ concentration
([Ca2+]i)
were measured with the fluorescent pH indicators seminaphthorhodafluor 1 and fluo 3, respectively, and contractility was assessed from changes
in cell shortening during field stimulation. Experiments were performed
at extracellular pH 7.4 in the presence and absence (HEPES buffer) of
CO2 and
HCO
3. Our findings demonstrate that
1) myocytes after myocardial
infarction (post-MI) were significantly larger than normal,
2) post-MI hypertrophy was not
accompanied by changes in non-CO2
intracellular buffering power, 3)
post-MI hypertrophy did not significantly affect the ability of
Na+/H+
exchange to mediate pHi recovery
from intracellular acidosis, 4) the
stimulatory effect of ANG II (100 nM) on
Na+/H+
exchange was significantly reduced in post-MI myocytes,
5) in HCO3-buffered solutions, ANG II did
not significantly stimulate pHi
recovery from acidosis in post-MI myocytes,
6) the angiotensin
AT1 receptor mediates the
stimulatory action of ANG II on
Na+/H+
exchange in normal and post-MI myocytes, and
7) the stimulatory effect of ANG II
on the Ca2+ transient and
contraction was blunted in post-MI myocytes bathed in HEPES-buffered
solution. A suppressed ventricular responsiveness to ANG II may be
beneficial in the intact myocardium by attenuating ATP consumption and
by reducing intracellular Na+
accumulation during ischemia-reperfusion.
acid extrusion; intracellular pH; contractility; sodium/hydrogen exchange
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