Verapamil potentiates vagally mediated sinoatrial chronotropic responses in dogs.
A brief burst of electrical stimuli delivered to the vagus nerve during the cardiac cycle elicits a triphasic cardiac chronotropic response. The cardiac cycle length initially increases, then briefly decreases, and subsequently increases again. We studied the effects of a calcium channel blocking agent, verapamil, on these responses to vagal stimulation during sinoatrial nodal rhythm in anesthetized, open-chest dogs. Verapamil increased the basal cardiac cycle length only slightly; however, the primary cardioinhibition was accentuated approximately 40% (from 396 to 555 ms) by verapamil. Neither the acceleratory phase of this triphasic response nor the secondary cardioinhibition was significantly affected by verapamil. These results indicate that verapamil potentiates the initial action of acetylcholine at the sinoatrial node when the vagus is activated with brief stimuli.
D000109:Acetylcholine / Q000502:physiology; D000818:Animals; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D012849:Sinoatrial Node / Q000187:drug effects*; D013268:Stimulation, Chemical; D014630:Vagus Nerve / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology*
D007473:Ion Channels; D014700:Verapamil; D000109:Acetylcholine; D011188:Potassium