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channel function in
guinea pig ventricular myocytes
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970
The role of
protein kinase C (PKC) in regulating the protein kinase A
(PKA)-activated Cl
current
conducted by the cardiac isoform of the cystic fibrosis transmembrane
conductance regulator (cCFTR) was studied in guinea pig ventricular
myocytes using the whole cell patch-clamp technique. Although
stimulation of endogenous PKC with phorbol 12,13-dibutyrate (PDBu)
alone did not activate this
Cl current, even when
intracellular dialysis was limited with the perforated patch-clamp
technique, activation of PKC did elicit a significant response in the
presence of PKA-dependent activation of the current by the
-adrenergic receptor agonist isoproterenol. PDBu
increased the magnitude of the
Cl conductance activated by
a supramaximally stimulating concentration of isoproterenol by 21 ± 3.3% (n = 9) when added after
isoproterenol and by 36 ± 16% (n = 14) when introduced before isoproterenol. 4
-Phorbol
12,13-didecanoate, a phorbol ester that does not activate PKC, did not
mimic these effects. Preexposure to chelerythrine or
bisindolylmaleimide, two highly selective inhibitors of PKC, significantly reduced the magnitude of the isoproterenol-activated Cl current by 79 ± 7.7% (n = 11) and 52 ± 10%
(n = 8), respectively. Our
results suggest that although acute activation of endogenous PKC alone
does not significantly regulate cCFTR
Cl channel activity in
native myocytes, it does potentiate PKA-dependent responses, perhaps
most dramatically demonstrated by basal PKC activity, which may play a
pivotal role in modulating the function of these channels.
bisindolylmaleimide; chelerythrine; cross talk; phorbol 12,13-dibutyrate; protein kinase C; cardiac isoform of cystic fibrosis transmembrane conductance regulator
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