A muscarinic receptor antagonist is an agent that reduces the activity of the muscarinic acetylcholine receptor. Most of them are synthetic, but scopolamine and atropine are belladonna alkaloids, and are naturally extracted.
It is stimulate CNS as a result of stimulation of medulla and higher cerebral centers. At low doses of atropine, causes slight restlessness; and at high or toxic doses it causes restlessness, agitation, hallucination. In atropine poisoning marked excitation and agitation leads to hyper activity and increased in body temperature by lose of sweating. Scopolamine in therapeutic doses causes CNS depression characterized by amnesia, fatigue and reduction in REM (Rapid Eye Movement) sleep. Hyoscine has anti-emetic activity, so used in motion sickness. Also used as anti-parkinsonian drug. In Parkinsonism, there is imbalance between Ach & dopamine occurs. In it there is increase level of Ach or degeneration of dopaminergic pathway (nigro-straital pathway). Thus, in Parkinsonism there is decrease level of dopamine. For, balancing the neurotransmitters, one treatment is considered that decrease level of Ach or decrease activity of Ach by MRA.
Effect on heart
Atropine acts on the M2-receptors of the heart and antagonized the activity of Ach. It causes tachycardia by blocking vagal effects on the SA node. Ach hyperpolarize the SA node which is over come by MRA and increase the heart rate. If atropine is given by intra muscular or sub cutaneous, it causes initial bradycardia. This is because; by i.m/s.c it acts on presynaptic M1-raceptors (auto receptors). So. The intake of Ach in axoplasm is prevented. Due to it, presynaptic nerve releases more Ach in to synapse which causes bradycardia, initially. At AV node, RP is abbreviated which facilitates conduction and also due to shortened PR-interval of ECG. It have alternative effect on BP. Due to tachycardia and stimulation of vasomotor centre causes increase in BP. But due to feed back regulation of VMC there is fall in BP due to vasodilation.
^ Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. Page 147
^ abc Unless else specified in table boxes, then ref is: Rang, H. P. (2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. Page 147
note: in PNS, ganglionic blocker can have direct antinicotinic action at preganglionic terminal, but simulate indirect antimuscarinic activities at postganglionic terminal
