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".
D000818:Animals; D003000:Clonidine / Q000031:analogs & derivatives* / Q000494:pharmacology; D003864:Depression, Chemical; D006168:Guinea Pigs; D006339:Heart Rate / Q000187:drug effects*; D066298:In Vitro Techniques; D054833:Isoindoles; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology*; D010797:Phthalimides / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology*; D012849:Sinoatrial Node / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology
D054833:Isoindoles; D009467:Neuromuscular Depolarizing Agents; D010797:Phthalimides; D014700:Verapamil; C022192:alinidine; D003000:Clonidine; C030532:falipamil; D011188:Potassium