Why the study?
Does the replacement of external sodium ions increase peak L-type calcium current in enzymatically isolated guinea pig ventricular cells?
Does the replacement of external sodium ions increase peak L-type calcium current in enzymatically isolated guinea pig ventricular cells?
This study provides first evidence that sodium ions modulate L-type calcium-channel phosphorylation via cAMP-dependent protein kinase.
Does not support changes to clinical ion channel management; leaves open sodium modulation of cardiac L-type currents for further study.
It is universally believed that the removal of external sodium ions is without effect on calcium current. We now report that in enzymatically isolated guinea pig ventricular cells, the replacement of external sodium ions with certain other cations causes a 3- to 6-fold increase in peak L-type calcium current. The increase in current is reversibly blocked by L-type calcium-channel antagonists, not mediated by changes in internal calcium, and is inhibited by intracellular 5'-adenylyl imidodiphosphate, a nonhydrolyzable ATP analogue. The effects of sodium removal (and isoproterenol) were almost completely blocked by intracellular application of a specific (peptide) inhibitor of cAMP-dependent protein kinase. These experiments demonstrate a previously unknown effect of sodium ions to modulate calcium-channel phosphorylation via cAMP-dependent protein kinase.
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Balke et al. (1992) studied this question.
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