Key result
Isoproterenol increased the delayed rectifier potassium current in guinea-pig ventricular cells, an effect that was abolished by intracellular application of GTP-gamma-S.
Why the study?
Does beta-adrenoceptor stimulation increase delayed rectifier potassium current via the adenylate cyclase/cAMP pathway in guinea-pig ventricular cells?
Does beta-adrenoceptor stimulation increase delayed rectifier potassium current via the adenylate cyclase/cAMP pathway in guinea-pig ventricular cells?
This study demonstrates that beta-adrenoceptor stimulation increases the delayed rectifier potassium current in ventricular cells through a G-protein and cAMP-dependent mechanism.
IIJIMA, T. and TAIRA, N. Mechanisms of β-Adrenoceptor Mediated Increase in Delayed Rectifier Potassium Current. Tohoku J. Exp. Med., 1989, 159 (4), 277-281 -Experiments were carried out in single ventricular cells of the guinea-pig heart. Isoproterenol, forskolin, intracellularly applied cyclic AMP and 3-isobutyl-1-methylxanthine increased the delayed rectifier potassium current (IK). The effect of isoproterenol was abolished by intracellularly applied guanosine 5'-O-(3-thio-triphosphate). These results indicate that isoproterenol stimulates β-adrenoceptors to activate adenylate cyclase by mediation through the stimulatory GTP-binding protein, and causes an increase in intracellular cyclic AMP levels. Then IK is probably increased by phosphorylation of the IK-channel protein by cyclic AMP-dependent protein kinase.
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Iijima et al. (1989) studied None (in vitro guinea-pig ventricular cells). Isoproterenol vs. Control (absence of drug) was evaluated on Delayed rectifier potassium current (IK). Isoproterenol increased the delayed rectifier potassium current in guinea-pig ventricular cells, an effect that was abolished by intracellular application of GTP-gamma-S.
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