Key result
Phenylarsine oxide transiently stimulated basal L-type Ca2+ channel activity via extracellular sulfhydryl oxidation and irreversibly inhibited PKA-dependent stimulation via an intracellular site.
Why the study?
Does phenylarsine oxide modulate basal and beta-adrenergically stimulated L-type Ca2+ channel activity in isolated cardiac myocytes?
Population
Isolated cardiac myocytes
Comparison
Phenylarsine oxide (PAO) vs Control/basal conditions
Design
Preclinical
Authors
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PAO redox effects on myocyte Ca channels warrant no clinical action; hypothesis-generating for beta-adrenergic modulation in cardiac disease.
Does phenylarsine oxide modulate basal and beta-adrenergically stimulated L-type Ca2+ channel activity in isolated cardiac myocytes?
The redox state of the cell, modulated by agents like PAO, plays a critical role in regulating the beta-adrenergic responsiveness of L-type Ca2+ channels in cardiac myocytes.
Sims et al. (2004) studied Isolated cardiac myocytes. Phenylarsine oxide (PAO) was evaluated on L-type Ca(2+) channel activity. Phenylarsine oxide transiently stimulated basal L-type Ca2+ channel activity via extracellular sulfhydryl oxidation and irreversibly inhibited PKA-dependent stimulation via an intracellular site.
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