Although a fifth muscarinic gene product (designated m5) has been cloned, no functional correlate for this receptor has been unambiguously demonstrated, and its pharmacology appears to differ from that of other muscarinic receptor subtypes. These correspond to the genetically cloned receptor subtypes m1-m4. The convention commonly used to classify muscarinic receptors designates pharmacologically defined muscarinic receptor subtypes as M 1, M 2, M 3, and M 4. There are considerable differences among antimuscarinics in the degree to which various pharmacologic effects are produced this may result in part from existence of 4 or more subtypes of muscarinic receptors. At high doses, quaternary ammonium antimuscarinics may produce substantial ganglionic blockade with resultant adverse effects (e.g., impotence, postural hypotension) and, in overdosage, they may cause a curariform neuromuscular block. However, quaternary ammonium antimuscarinics generally possess varying degrees of nicotinic blocking activity and may interfere with ganglionic or neuromuscular transmission at doses that block muscarinic receptors. At the neuromuscular junction, where cholinergic receptors are principally or exclusively nicotinic, only extremely high doses of atropine or other tertiary amine antimuscarinics produce any degree of blockade. Since the functions antagonized by antimuscarinics principally are under the parasympathetic division of the nervous system, these drugs also have been referred to as parasympatholytics.Īt autonomic ganglia, where cholinergic transmission involves nicotinic receptors, atropine or other tertiary amine antimuscarinics produce a partial cholinergic block only at relatively high doses. Antimuscarinics also have been referred to as anticholinergics (cholinergic blocking agents), but this term is appropriate only when it describes the antagonism of cholinergic stimuli at any cholinergic receptor, whether muscarinic or nicotinic. These drugs are referred to as antimuscarinics because at usual doses they principally antagonize cholinergic stimuli at muscarinic receptors and have little or no effect on cholinergic stimuli at nicotinic receptors. Last revised: November 2011Īntimuscarinics competitively inhibit the actions of acetylcholine or other cholinergic stimuli at autonomic effectors innervated by postganglionic cholinergic nerves, and to a lesser extent, on smooth muscles that lack cholinergic innervation. Product Label: ATROPINE SULFATE injection Following clinical and larger doses, atropine sulfate causes dilation of the pupils and paralysis of accommodation and in narrow-angle glaucoma, can increase intraocular pressure. These actions include vasodilation, drying of the mouth, an increase in the pulse rate, inhibition of contractions of the gastrointestinal tract, ureter, and bladder, and reduction of salivary, bronchial, gastric and sweat gland secretions. It does not prevent the release of acetylcholine but antagonizes the effect of acetylcholine on the effector cells. Atropine sulfate also acts peripherally as a competitive antagonist of the muscarinic actions of acetylcholine. This effect is manifested by mild central vagal excitation and moderate respiratory stimulation. Following the administration of usual clinical doses, atropine produces stimulation of the medulla and higher cerebral centers. It also has central nervous system activity, which may be stimulating or depressing depending upon the dose. The most important therapeutic action of atropine is the inhibition of smooth muscle and glands innervated by postganglionic cholinergic nerves. Evidence-based medicine for Chemical Defense - including efficacy and safety A. Chemical Defense therapeutic area(s) - including key possible usesĪtropine Sulfate is used for treatment of nerve agent poisoning and organophosphate pesticide poisoning. Name of Chemical Defense therapeutic agent/deviceĪtropine Sulfate 2.
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