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Muscarinic effects acetylcholine

MONOAMINES dopamine j norepinephrine / epinephrine serotonin (5HT) acetylcholine (muscarinic effects)... [Pg.50]

Exposure to disulfoton can result in inhibition of acetylcholinesterase activity, with consequent accumulation of acetylcholine at nerve synapses and ganglia leading to central nervous system, nicotinic, and muscarinic effects (see Section 2.2.1.4 for more extensive discussion). [Pg.76]

The N-methyl carbamate esters cause reversible carbamylation of the acetylcholinesterase enzyme, allowing accumulation of acetylcholine, the neuromediator substance, at parasympathetic neuroeffector junctions (muscarinic effects), at... [Pg.75]

Pharmacology Direct-acting miotics are parasympathomimetic (cholinergic) drugs which duplicate the muscarinic effects of acetylcholine. When applied topically, these drugs produce pupillary constriction, stimulate ciliary muscles, and increase aqueous humor outflow facility. With the increase in outflow facility, there is a decrease in lOP. Topical ophthalmic instillation of acetylcholine causes no discernible P.1248... [Pg.2087]

The action of administered acetylcholine on effector systems innervated by parasympathetic postganglionic neurons (smooth muscle cells, cardiac muscle cells, and exocrine gland cells) resembled the actions produced by the naturally occurring plant alkaloid muscarine. The actions of both acetylcholine and muscarine on the visceral effectors are similar to those produced by parasympathetic nerve stimulation. Furthermore, the effects of acetylcholine, muscarine, and parasympathetic nerve stimulation on visceral effectors are antagonized by atropine, another plant alkaloid. [Pg.92]

Mechanism of Action An acetylcholine antagonist that inhibits the action of acetylcholine by competing with acetylcholine for common binding sites on muscarinic receptors, which are located on exocrine glands, cardiac and smooth-muscle ganglia, and intramural neurons. This action blocks all muscarinic effects. Therapeutic Effect Decreases GI motility and secretory activity, and GU muscle tone (ureter, bladder) produces ophthalmiccycloplegia, and mydriasis. [Pg.101]

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... [Pg.29]

The alkaloids namely atropine, hyoscyamine and scopolamine are obtained from Atropa belladonna. Atropine is dl-hyoscyamine, and, 1-isomer is more potent than d-form both peripherally and centrally. Atropine blocks the muscarinic effects of acetylcholine, the antagonism between acetylcholine and atropine is of competitive... [Pg.161]

The toxic effects can be divided into three types as the accumulation of acetylcholine leads to symptoms that mimic the muscarinic, nicotinic, and CNS actions of acetylcholine. Muscarinic receptors for acetylcholine are found in smooth muscles, the heart, and exocrine glands. Therefore, the signs and symptoms are tightness of the chest, wheezing due to bronchoconstriction, bradycardia, and constriction of the pupils (miosis). Salivation, lacrimation, and sweating are all increased, and peristalsis is increased, leading to nausea, vomiting, and diarrhea. [Pg.346]

The miotic effects of carbachol and bethanechol are greater than those of acetylcholine. Atropine is able to antagonize all cholinergic (muscarinic) effects produced by acetylcholine, methacholine, carbachol, and bethanechol. However, this antagonism is least evident with carbachol. [Pg.374]

The family of G proteins contains several functionally diverse subfamilies (Table 2-2), each of which mediates effects of a particular set of receptors to a distinctive group of effectors. Receptors coupled to G proteins comprise a family of "seven-transmembrane" or "serpentine" receptors, so called because the receptor polypeptide chain "snakes" across the plasma membrane seven times (Figure 2-11). Receptors for adrenergic amines, serotonin, acetylcholine (muscarinic but not... [Pg.33]

Carbamates effect the reversible carbamylation of acetylcholinesterase, permitting accumulation of acetylcholine at cholinergic neuroeffector junctions (muscarinic effects), at the myoneural junctions of skeletal muscle, and in the autonomic ganglia (nicotinic effects). CNS function is also impaired. However the relatively large dissociation constant of the carbamyl-enzyme complex indicates that it dissociates more readily than does the organophosphate-enzyme complex, mitigating the toxicity of the carbamate pesticides. The reversibility of the carbamyl-enzyme complex affects (limits) the utility of blood enzyme measurements as a diagnostic tool. [Pg.393]

Figure 9.10 shows two agonists that act selectively on muscarinic s5mapses Muscarine (surprise ) and pilocarpine. Both of these compounds have rather remote similarity with each other or with acetylcholine. Muscarine does not have an ester bond and is active orally. It is, however, not used therapeutically - rather, it is a poison found in toadstool and other mushrooms. It will produce the effects -bronchial constriction, hypersalivation, intestinal cramps -... [Pg.83]

Cholinergic drugs (acetylcholine agonists) mimic acetylcholine at all sites although the balance of nicotinic and muscarinic effects is variable. [Pg.433]

Choline esters (carbachoi, bethanechol) which act at all sites like acetylcholine. They are resistant to degradation by cholinesterases. Muscarinic effects are much more prominent than nicotinic (see p. 435). [Pg.433]

Metrifonate, which is given orally, is effective in Schistosoma hematobium infections in three doses of 7.5-10 mg/kg 14 days apart. When metrifonate was used in daily doses, as in the treatment of Onchocerca volvulus infections, it produced muscarinic effects, and in one case there was proximal weakness due to a nicotinic effect. The combination of polyarthritis, fever, and a raised sedimentation rate was described in 11 of 34 patients treated. Metrifonate inhibits blood cholinesterase activity for up to 48 hours, and common reactions that probably result from this effect comprise nausea, vomiting, abdominal pain, diarrhea, dizziness, weakness, headache, and muscle cramps. Because of its prolonged inhibition of brain cholinesterase and increased steady-state concentrations of acetylcholine in the cortex and the hippocampus, it is now also increasingly used in the treatment of Alzheimer s disease. [Pg.2321]

Muscarinic effects, mediated by acetylcholine, the primary transmitter of the autonomic nervous system ganglia, are inhibited by the anticholinergic effects exerted by antihistamines. Anticholinergic side effects include dry mouth, urinary retention, blurred vision, and constipation. Because first-generation antihistamines also distribute into the CNS, sedation is a prominent side effect. The development of second-generation antihistamines, such as loratadine and fexofenadine, lack anticholinergic activity and do not distribute into the CNS (Table 31-1). Hence, they are not typically associated with sedation and do not possess antiemetic properties. [Pg.73]

The clinical signs of excess acetylcholine at nerve endings mimic hyperactivity of the parasympathetic nervous system. Signs relative to the alimentary tract include excess salivation, lacrimation, abdominal pain, vomiting, intestinal hypermotility, and diarrhea. The muscarinic effects of acetylcholine cause bronchoconstriction and an increase in bronchial secretions. The nicotinic effects of acetylcholine consist of involuntary irregular, violent muscle contractions and weakness of voluntary muscles. Death occurs as a result of respiratory failure. [Pg.33]


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See also in sourсe #XX -- [ Pg.25 , Pg.37 , Pg.46 ]

See also in sourсe #XX -- [ Pg.27 , Pg.90 , Pg.152 , Pg.413 , Pg.425 , Pg.484 , Pg.499 , Pg.525 ]




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