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
Heart development before the fusion of the endocardial tubes. The heartbeat begins in the region of the pacemaker which has a spontaneous depolarization time faster than the rest of myocardium. The primitive ventricle acts as initial pacemaker. But this pacemaker activity is actually made by a group of cells that derive from the sinoatrial right venous sinus. These cells form an ovoid sinoatrial node (SAN), on the left venous valve. After the development of the SAN, the superior endocardial cushions begin to form a pacemaker as known as the atrioventricular node. With the development of the SAN, a band of specialized conducting