Muscarinic antagonist brain, involving both increased levels of acetylcholine and degeneration of dopaminergic pathways (nigrostriatal pathway). Thus, in parkinsonism there is decreased level of dopaminergic activity. One method of balancing the neurotransmitters is through blocking central cholinergic activity using muscarinic receptor antagonists. Atropine acts on the M2 receptors of the heart and antagonizes the activity of acetylcholine. It causes tachycardia by blocking vagal effects on the sinoatrial node. Acetylcholine hyperpolarizes the sinoatrial node, which is overcome by MRA and thus increases the heart rate. If atropine is given by intramuscular or subcutaneous injection, it causes initial bradycardia. This is because by i.m/s.c
Sinoatrial block lengthening of conduction time from the SA node to the atria. The p-cells in the centre of the node produce the rhythm at a regular rate, but their conduction across the node to where it meets atrial tissue is where the slowing occurs. A second degree type II, or sinus exit block, is a regular rhythm that may be normal or slow. It is followed by a pause that is a multiple of the P-P interval usually (2-4) . Conduction across the SA node is normal until the time of the pause when it is blocked. A third degree sinoatrial