Autonomous block

The newer H -antagonists such as terfenadine and astemizole are claimed to have little or no sedative action. Astemizole is also claimed to be free of autonomic blocking effects. Loratidine is claimed to have little autonomic and CNS blocking effects. 

Unlike antipsychotic or antidepressant drugs, which exert several actions on the central or autonomic nervous system, lithium ion at therapeutic concentrations is devoid of autonomic blocking effects and of activating or sedating effects, though it can produce nausea and tremor. 

Durant NN, Marshall IG, Savage DS, Nelson DJ, Sleigh T, Carlyle IC. The neuromuscular and autonomic blocking activities of pancuronium, Org NC 45, and other... 

Drugs that block the nicotinic receptors on autonomic ganglia, such as hexamethonium, probably do so by actually blocking the Na+ ion channel rather than the receptor. Generally these receptors appear to resemble the central ones more than those at the neuromuscular junction and dihydro-jS-erythroidine is one drug that it is an effective antagonist in both ganglia and the CNS. 

Mailer I have some speculations. The other thing that goes on in an embryo that is independent of protein synthesis is centrosome replication. We showed last year that if cyclin E/Cdk activity is blocked, so is centrosome replication. One possibility is that the timer is actually monitoring centrosomes, as a sort of autonomous thing that replicates. The two things that are replicated in cells are the genome and centrosomes very little is known about centrosome replication. 

The answers arc 488-d, 489-h. (Katzang, pp 108-112, 1020.) Atropine blocks muscarinic cholinergic transmission in the brain and in the autonomic nervous system. The result is dry mouth, thirst, dry and hot skin, tachycardia, urinary retention, ataxia, restlessness, excitement, and hallucinations, followed by stupor, delirium, respiratory depression, coma, and death. 

Delayed-action paralytic neurotoxins that block the release of acetylcholine causing a symmetric, descending flaccid paralysis of motor and autonomic nerves. Paralysis always begins with the cranial nerves. Toxins are obtained from an anaerobic bacteria (Clostridium botulinum). Toxin A is a white powder or crystalline solid that is readily soluble in water. It is stable for up to 7 days as an aqueous solution. All toxins are destroyed by heat and decompose when exposed to air for more than 12 h. 

Neurotransmission in autonomic ganglia is more complex than depolarization mediated by a single transmitter 190 Muscarinic receptors are widely distributed at postsynaptic parasympathetic effector sites 190 Stimulation of the motoneuron releases acetylcholine onto the muscle endplate and results in contraction of the muscle fiber 191 Competitive blocking agents cause muscle paralysis by preventing access of acetylcholine to its binding site on the receptor 191... 

We will conclude this chapter by referring to a term often used for those symptomatic drugs inhibiting the action of the autonomic nervous system by interfering with the effect of the chemical mediators involved. There are two groups. (1) Para-sympatholytic drugs block the action of acetylcholine. These are included within the wider class of spasmolytics which, as the name suggests, check or eliminate spasms. (2) Sympatholytics inhibit the action of adrenaline, noradrenaline and the sympathetic nervous system. 

Pharmacologically, the properties of all three alkaloids are very similar, except y-coniceine is more stimulatory to autonomic ganglia and VV-methyl coniine has a greater blocking effect (Fodor and Colasanti, 1985). 

These agents inhibit the muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites including smooth muscle, secretory glands, and CNS sites. Large doses may block nicotinic receptors at the autonomic ganglia and at the neuromuscular junction. 

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