Muscarine-like action

Muscarine-like action causing bronchospasm atropine and ephedrine are antagonists. Other parasympathetic effects include constriction of the pupil and of the ciliary muscles of the eye both effects are antagonized by atropine. 

Muscarinic agonist A cholinomimetic drug with primarily muscarine-like actions... 

This view was supported by the observation that choline on treatment with nitric acid yielded a product having a pharmacological action similar to that of muscarine as known up to that time. Comparison of the natural and artificial products by Bohm showed that the former was much more active than the latter and that its action was antagonised by atropine, whilst the artificial muscarine had a curare-like action on the atropinised frog. Later, Nothnagel investigated the action of... 

Receptor interactions were seen at nicotinic and muscarinic receptors. No correlations were found, however, between atropinelike or curare-like actions of these compounds and their protective effects against organophosphate poisoning. 

Muscarinic Receptor Interactions. Excitatory muscarinic effects, such as temporary stimulation of salivation and stimulation of intestinal peristalsis, were seen with 2-PAM. Atropine-like actions were seen at high concentrations (15-20 mg/kg or more), and, when injected rapidly, 2-PAM caused temporary diplopia (nicotinic block) and loss of accommodation in the eye.Both TMB-4 and 2-PAM blocked bradycardia induced by vagal stimulation. At low concentrations, neither compound affected normal intestinal peristalsis, but they did block peristalsis caused by increased vagal stimulation. TMB-4, 2-PAM, and toxogonin antagonized the effect of acetylcholine, acetyl- -methyl-choline, and other agonists on Isolated guinea pig ileum.62... 

Administered hypodermically to animals it causes muscarine-like intoxication, although much less mtense in its action than either that alkaloid or neurine ... 

The principal pharmacodynamic action of atropine is the role it plays on substances exerting a muscarine-like effect. It opposes the effects of acetylcholine, whether they be motor, inhibitor, or secretory in action. Thus atropine inactivates a stimulation of the parasympathetic nervous system. The first observations on this subject date from 1867 (119). 

Aspirin, sympathomimetics, agents with muscarinic blocking actions, and drugs that cause muscle rigidity or seizures are all likely to cause hyperthermia at toxic doses. Hypothermia is more typical of overdoses with opioids or sedative-hypnotics. The answer is (C). 

In addition to natural muscarine and the so-called choline-muscarine referred to above, two other products have been given names suggesting relationship to muscarine, viz. (1) isomuscarine, Me3N(OH). CHOH. CH2OH prepared by Bode and shown to be toxic, but distinct from muscarine in type of action, and (2) anhydromuscarine (betaine aldehyde) made first by Berlinerblau and later by Fischer and which, according to Voet possesses nicotine and curare-like properties. 

In contrast to the nicotinic antagonists and indeed both nicotinic and muscarinic agonists, there are a number of muscarinic antagonists, like atropine, hyoscine (scopolamine) and benztropine, that readily cross the blood-brain barrier to produce central effects. Somewhat surprisingly, atropine is a central stimulant while hyoscine is sedative, as least in reasonable doses. This would be the expected effect of a drug that is blocking the excitatory effects of ACh on neurons but since the stimulant action of atropine can be reversed by an anticholinesterase it is still presumed to involve ACh in some way. Generally these compounds are effective in the control of motion but not other forms of sickness (especially hyoscine), tend to impair memory (Chapter 18) and reduce some of the symptoms of Parkinsonism (Chapter 15). 

Many measurements in pharmacology rely on a chain of events following receptor activation to produce a measurable response — for example, contraction of the smooth muscle of a piece of guinea-pig ileum in response to muscarinic receptor activation by acetylcholine. This means that the relationship between receptor occupancy and response is likely to be complex, and mechanisms of drug action in such systems are often difficult to define. 

The efficacy of anticholinergic drugs in parkinsonism is likely due to the ability to block muscarinic receptors in the striatum. In the absence of the inhibitory action of dopamine, the actions of the intrastriatal cholinergic interneurons are unopposed, yielding enhanced stimulation of muscarinic receptors. Blockade of these receptors reduces striatal activity. The muscarinic antagonists exert only modest antiparkinsonian actions and thus are most commonly used during the early stages of the disease or as an adjunct to levodopa therapy. 

Many first-generation agents, especially those of the ethanolamine and ethylenediamine subgroups, have significant atropine-like effects on peripheral muscarinic receptors. This action may be responsible for some of the (uncertain) benefits reported for nonallergic rhinorrhea but may also cause urinary retention and blurred vision. 

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