Acetylcholine prolonged

CgHijClNjOj. Colourless, hygroscopic, m.p. 2I0-212 C (decomp.). Prepared from fi-chloroethyl carbamate and trimethylamine. It has a physiological action similar to that of acetylcholine, but more prolonged, as it is less readily hydrolysed. It is used for intestinal atony following operations, and can be given orally. 

The Class I agents decrease excitability, slow conduction velocity, inhibit diastoHc depolarization (decrease automaticity), and prolong the refractory period of cardiac tissues (1,2). These agents have anticholinergic effects that may contribute to the observed electrophysiologic effects. Heart rates may become faster by increasing phase 4 diastoHc depolarization in SA and AV nodal cells. This results from inhibition of the action of vagaHy released acetylcholine [S1-84-3] which, allows sympathetically released norepinephrine [51-41-2] (NE) to act on these stmctures (1,2). 

The release of some peptides may differ from that of other transmitters, depending on the firing rate of the neurons. The large vesicles needed to store a peptide may need a greater rate of depolarisation for membrane fusion and release of the contents. In the salivary gland the release of vasoactive intestinal polypeptide requires high-frequency stimulation whereas acetylcholine is released by all stimuli. Due to the complexities and problems of access to CNS synapses it is not known if the same occurs here but there is no reason why this should not. In sensory C-fibres a prolonged stimulus appears to be a prerequisite for the release of substance P. 

Mitsis, E.M., van Dyck, C.H., Krantzler, E. et al. Prolonged occupancy of nicotinic acetylcholine receptors by nicotine in human brain a preliminary study. Paper presented at the Annual Meeting of the Society for Research on Nicotine and Tobacco, Orlando, FL, 2006. 

Anticholinesterase A drug that inhibits the enzyme acetylcholinesterase, which normally inactivates acetylcholine at the synapse. The effect of an anticholinesterase (or cholinesterase inhibitor) is thus to prolong the duration of action of the neurotransmitter. An example is rivastigmine, used in the treatment of Alzheimer s disease. 

The snbgronps of muscarinic receptors (Mj and M2) are activated or blocked by various substances however, both types of muscarinic receptors are activated by an endogenic nenrotransmitter—acetylcholine—and are blocked by atropine or scopolamine. Despite the fact that atropine and scopolamine are reversible cholinoblocking agents, the constants of their dissociation with M-receptors are several times less than acetylcholine. Accordingly, their action is more prolonged (for a few days). 

The resultant elevation of acetylcholine causes a transient period of contraction followed by prolonged depolarization in the postsynaptic muscle cell, which induces relaxation and then paralysis of the victim. 

Atropine, a tertiary amine, competitively antagonizes acetylcholine activity. Full therapeutic doses of atropine produce definite and prolonged inhibitory effects on the motor activity of the stomach, duodenum, jejunum, ileum, and colon, characterized by a decrease in tone and in amplitude and frequency of peristaltic contractions. 

Mechanism of Action A cholinesterase inhibitor that enhances and prolongs cholinergic function by increasing the concentration of acetylcholine through inhibition of f he hydrolysis of acefylcholine. Therapeutic Effect Increases muscle strength in myasthenia gravis. 

Mechanism of Action Competitive inhibitors of the muscarinic actions of acetylcholine, acting at receptors located in exocrine glands, smooth and cardiac muscle, and intramural neurons. Composed of 3 main constituents atropine, scopolamine, and hyoscyamine. Scopolamine exerts greater effects on the CNS, eye, and secretory glands than the constituents atropine and hyoscyamine. Atropine exerts more activity on the heart, intestine, and bronchial muscle and exhibits a more prolonged duration of action compared to scopolamine. Hyoscyamine exerts similar actions to atropine but has more potent central and peripheral nervous system effects. TherapeuticEffect Peripheral anticholinergic and antispasmodic action, mild sedation. Pharmacokinetics None known... 

The pharmacological effects are those of acetylcholine. It produces prolonged inhibition of true and pseudocholinesterases. They are inactivated in the body completely by oxidation and hydrolysis and excreted in urine. 

The cholinesterase inhibitors have important therapeutic and toxic effects at the skeletal muscle neuromuscular junction. Low (therapeutic) concentrations moderately prolong and intensify the actions of physiologically released acetylcholine. This increases the strength of contraction, especially in muscles weakened by curare-like neuromuscular blocking agents... 

At least two additional types of acetylcholine receptors are found within the neuromuscular apparatus. One type is located on the presynaptic motor axon terminal, and activation of these receptors mobilizes additional transmitter for subsequent release by moving more acetylcholine vesicles toward the synaptic membrane. The second type of receptor is found on perijunctional cells and is not normally involved in neuromuscular transmission. However, under certain conditions (eg, prolonged immobilization, thermal burns), these receptors may proliferate sufficiently to affect subsequent neuromuscular transmission. 

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