Heart

Intravenous administration of low doses of atropine or scopolamine often produces slight bradycardia, whereas higher doses produce tachycardia by directly blocking the parasympathetic input to the sinoatrial node. Although it has been suggested that the bradycardia results from an effect of the drugs on the CNS (thought to be central vagal stimulation), this appears unlikely, since methylatropine (a quaternary ammonium derivative of atropine) produces a similar response. One plausible explanation for the paradoxical bradycardia produced by low doses of muscarinic blockers is that they block presynaptic muscarinic receptors that normally provide feedback inhibition of the release of ACh. Antagonism of these presynaptic muscarinic receptors prevents feedback inhibition and increases the release

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