Sweating, muscarinic receptors

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

The oral cholinergic agonists pilocarpine and cevimeline are used for patients with combined dry eye and dry mouth (e.g., Sjogren s syndrome) or severe dry eye. By binding to muscarinic receptors, the cholinergic agonists may increase tear production. Excessive sweating is a common side effect with pilocarpine and may limit its use (Table 60-10). 

Muscarine, an alkaloid from certain species of mushrooms, is a muscarinic receptor agonist. The compound has toxicologic importance muscarine poisoning will produce all of the effects that are associated with an overdose of ACh (e.g., bronchocon strict ion, bradycardia, hypotension, excessive salivary and respiratory secretion, and sweating). Poisoning by muscarine is treated with atropine. 

Muscarinic receptors are responsible for postganglionic parasympathetic neurotransmission and thus for control of a wide range of smooth muscle, cardiac muscle and secretory responses. Some responses originating in the sympathetic division of the autonomic nervous system, such as sweating and piloerection, also are mediated through muscarinic receptors. 

Atropine, an alkaloid from Atropa belladonna, is the classical parasympatholytic compound. It competes with acetylcholine for the binding at the muscarinic receptor. Its affinity towards nicotinic receptors is very low, so that it does not interfere with the ganglionic transmission or the neuromotor transmission, at least in therapeutic dosages. However, in the central nervous system muscarinic receptor do play an important role and while atropine can penetrate the blood-brain barrier it exerts pronounced central effects. Atropine, like all other antagonists of the muscarinic acetylcholine receptor inhibit the stimulatory influence of the parasympathetic branch of the autonomous nervous system. All excretory glands (tear, sweat, salivary, gasto-intestinal, bronchi) are... 

Mechanism of Action A G1 ant ispasmodic and ant ichol inergic agent that inhibits the action of acetylcholine at postganglionic (muscarinic) receptor sites. Therapeutic Effect Decreases secretions (bronchial, salivary, sweat gland) and gastric juices and reduces motility of G1 and urinary tract. 

Stimulation of the parasympathetic nervous system modifies the organ functions by two main pathways. Firstly, the acetylcholine released from parasympathetic nerves can activate muscarinic receptors which are present in gland cells (sweat glands), smooth muscles and heart. The... 

Atropine suppresses thermoregulatory sweating. Sympathetic cholinergic fibers innervate eccrine sweat glands, and their muscarinic receptors are readily accessible to antimuscarinic drugs. In adults, body temperature is elevated by this effect only if large doses are administered, but in infants and children even ordinary doses may cause "atropine fever."... 

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. 

Sweating is stimulated by direct action of the increased endogenous acetylcholine on muscarinic receptors of sweat glands in the skin these glands are innervated by the sympathetic division of the autonomic nervous system. Agitation is produced by a central excitatory effect on cholinergic neurones in the brain, but in large doses anticholinesterases can cause depression of the respiratory centre in the medulla. 

Q10 Atropine would be a suitable antagonist to the effects of the anticholinesterase at muscarinic receptors and would reverse the intestinal cramps, lacrimation, drooling, sweating and so on, since atropine is a muscarinic antagonist. So atropine can be considered as an antidote . 

Reboxetine is a selective noradrenaline re-uptake inhibitor with low affinity for a-adrenoceptors and muscarinic receptors. In controlled trials the following adverse events occurred significantly more often with reboxetine than with placebo dry mouth (27%), constipation (17%), increased sweating (14%), insomnia (14%), urinary... 

Muscarinic receptors play an essential role in regulating the functions of organs innervated by the autonomic nervous system to maintain homeostasis of the organi.sm. The action of ACh on muscarinic receptors con re.sull in. stimulation or inhibition of the organ system affected. ACh stimulates secretions from salivary and sweat glands, secretions and contraction of the gut. and constriction of the airways of the respiratory tract. It inhibits contraction of the heart and relaxes smooth muscle of blood vc.ssels. 

BZ is a competitive inhibitor of muscarinic receptors associated with the parasympathetic nervous system that innervate the eyes, heart, respiratory system, skin, gastrointestinal tract, and bladder. The sweat glands, innervated by the sympathetic nervous system, are also modulated by muscarinic receptors. By any route of exposure, the onset of action is approximately 1 h, with peak effects occurring 8h postexposure. Signs and symptoms gradually subside over 2-4 days. Most of the absorbed BZ is excreted via the kidney. 

M 3—Muscarinic receptors are located on all organs and tissues innervated by postganglionic nerves of the PANS and on thermoregulatory sweat glands innervated by the SANS. 

Major cholinergic alkaloid derived from the lab-orandi plant from its leaves. Acts on muscarinic receptors sweating, salivation, flushing, lachry-mation, tachycardia. 

Of direct relevance for pesticide science is the antagonist atropine. This toxicant also binds specifically to the muscarinic receptors where it blocks the effect of ACh. The symptoms are therefore the opposite of those caused by muscarine or acetylcholine (pupil dilation, dry mouth, inhibition of sweating, tachycardia, palpitations, hallucinations, delirium, etc.). Atropine is an important antidote when one is poisoned with a cholinesterase-inhibiting insecticide. 

Pilocarpine is administered orally in 5-10-mg doses given three times daily for the treatment of xerostomia that follows head and neck radiation treatments or that is associated with Sjogren s syndrome, an autoimmune disorder occurring primarily in women in whom secretions, particularly salivary and lacrimal, are compromised. Side effects typify cholinergic stimulation, with sweating being the most common complaint. Bethanechol is an oral alternative that produces less diaphoresis. Cevimeline (evoxac) has activity at M muscarinic receptors, such as those on lacrimal and salivary... 

Uninnervated receptors Some receptors that respond to autonomic transmitters and drugs receive no innervation. These include muscarinic receptore on the endothelium of blood vessels, some presynaptic receptors, and, in some species, the adrenoceptors on apocrine sweat glands and a, and P adrenoceptors in some blood vessels. 

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