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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Decrease in bradycardic effect of AQ-A 39 and alinidine in guinea-pig sinoatrial node depolarized by high external K+-concentration.

The effects of the two "specific bradycardic agents" AQ-A 39 and alinidine on the spontaneous electrical discharge rate of intact guinea-pig sinus node preparations were investigated. At high external K+-concentrations (10.8 and 16.2 mmol/l) the bradycardic effect of the two drugs was diminished or abolished. In contrast, the negative chronotropic effect of the reference compound verapamil ("Ca2+-antagonist") was enhanced. These results show that the bradycardic effects of AQ-A 39 and alinidine are diminished in depolarized preparations, which makes it unlikely that in intact sinus node preparations the mechanism of action is the same as that of "Ca2+-antagonists".[1]

References

  1. Decrease in bradycardic effect of AQ-A 39 and alinidine in guinea-pig sinoatrial node depolarized by high external K+-concentration. Lillie, C., Kobinger, W. Naunyn Schmiedebergs Arch. Pharmacol. (1984) [Pubmed]
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