No abstract available.
Phenylephrine* ; Receptors, Cholinergic* ; Vas Deferens*

No abstract available.
Colon ; Interstitial Cells of Cajal ; Receptors, Cholinergic

Cholinergic urticaria with acquired generalized hypohidrosis, and its pathophysiology is not well known. Autoimmunity to sweat glands or to acetylcholine receptors on sweat glands has been mentioned as one of the possible etiologies. Systemic steroid therapy, antihistamines, anticholinergics, and avoidance of the stimulatory situations are recommended for treatment. We experienced a case of cholinergic urticaria with acquired generalized hypohidrosis in a patient who had no other associated disease, and the symptoms eased after repeated bilateral stellate ganglion block. Stellate ganglion block normalized the elevated sympathetic tone and may relieve symptoms in patients with this condition.
Autoimmunity ; Cholinergic Antagonists ; Histamine Antagonists ; Humans ; Hypohidrosis ; Receptors, Cholinergic ; Stellate Ganglion ; Sweat Glands ; Urticaria

Basal Forebrain ; Cholinergic Agents ; Cholinergic Neurons ; Humans ; Receptors, Histamine H1 ; Schizophrenia

Autoantibodies ; Calcium Channels ; Humans ; Myasthenia Gravis ; Receptors, Cholinergic/metabolism*

BACKGROUND: Intrathecal gabapentin is effective on nociceptive states evoked by tissue injury. In addition, gabapentin interacts synergistically with clonidine at the spinal level, suggesting that a mechanism of gabapentin may be related to spinal adrenoceptors. However, it has not been established whether this drug is associated with cholinergic receptors. The aim of this study was to examine the role of spinal adrenergic and cholinergic receptors on the antinociceptive action of intrathecal gabapentin. METHODS: Rats were implanted with lumbar intrathecal catheters. For a nociceptive test, 50nl of 5% formalin solution was injected into the hindpaw. The effect of intrathecal gabapentin, administered 10 min before the formalin injection, was assessed. Next, antagonistic effects of intrathecal prazosin, yohimbine, atropine and mecamylamine for the action of intrathecal gabapentin were evaluated. RESULTS: Formalin injection caused a biphasic incidence of flinching of the injected paw. Intrathecal gabapentin produced a dose-dependent suppression of only the phase 2 flinching response in the formalin test. Intrathecal atropine, but not prazosin, yohimbine nor mecamylamine, reversed the antinociception of intrathecal gabapentin. CONCLUSIONS: The antinociceptive effect of intrathecal gabapentin on facilitated states may be mediated through the muscarinic receptor but by neither the nicotinic receptor nor the adrenergic receptor at the spinal level.
Animals ; Atropine ; Catheters ; Cholinergic Antagonists* ; Clonidine ; Formaldehyde ; Incidence ; Mecamylamine ; Nociception ; Pain Measurement ; Prazosin ; Rats ; Receptors, Adrenergic ; Receptors, Cholinergic ; Receptors, Muscarinic ; Receptors, Nicotinic ; Spinal Cord ; Yohimbine

Effects of several autonomic drugs on the responses of the isolated rabbit detrusor muscle strips to electrical stimulation were investigated. Electric stimulation of the detrusor muscle strips elicited two different responses; (a) contraction followed by relaxation in 14 cases out of 22 experiments, and (b) contraction only in 8 cases. The contraction responses to electrical stimulation were significantly reduced in the presence of either atropine or regitine, respectively The relaxation response to electrical stimulation was abolished in the presence of propranolol. Addition of norepinephrine evoked one of following three responses: (a) relaxation in 10 cases out of 19 experiments, (b) contraction in 6 cases, and (c) contraction followed by relaxation in 4 cases. The relaxation response to norepinephrine was reversed. in the presence of propranolol, to a contraction response which was then abolished after administration of regitine. The contraction response to norepinephrine was reversed, in the presence of regitine, to a relaxation response which was then abolished after administration of propranolol. Acetylcholine elicited contraction of the isolated detrusor muscle strip, and this was abolished in the presence of atropine These results suggest that the rabbit detrusor muscle is innervated by both cholinergic and adrenergic fibers and that the detrusor muscle contains cholinergic receptors as well as adrenergic a-and b-ones. Contrary to the popular opinion that the detrusor muscle predominantly contains adrenergic b-receptors, it seems likely that the adrenergic receptors differ in predominancy of either a or b which elicits contraction or relaxation, respectively, according to different areas of the muscle.
Acetylcholine ; Adrenergic Fibers ; Atropine ; Autonomic Agents* ; Electric Stimulation* ; Norepinephrine ; Phentolamine ; Propranolol ; Receptors, Adrenergic ; Receptors, Cholinergic ; Relaxation

Major classes of medication in asthma management include bronchodilating beta2-agonists, anti-inflammatory inhaled corticosteroids, leukotriene modifiers and theophyllines. However, all asthmatics do not respond to the same extent to a given medication. Available data suggest that a substantial range of individual variability, as much as 70%, may be due to genetic characteristics of each patient. Pharmacogenomics offers the potential to optimize medications for individual asthmatics by using genetic information to improve efficacy or avoid adverse effects. The best-studied case of the potential contribution of pharmacogenomics to treatment response in asthma comes from studies on human beta2 adrenergic receptors. In addition, genetic variation in beta2-adrenergic receptor (Arg16Gly) may predict response to anticholinergics for the treatment of asthma. In case of inhaled corticosteroids, a recent investigation using a traditional SNP-based approach identified a gene for corticotropin releasing hormone receptor 1 as a potential marker of response. Another major pathway that has been investigated is the pathway underlying response to cysteinyl leukotriene receptor antagonist. It is likely that in the near future, pharmacogenomic approaches based on individual genetic information will be introduced into an asthma treatment guideline and this guideline will allow us to identify those who have the best chance to respond to a specific medication.
Adrenal Cortex Hormones ; Asthma ; Cholinergic Antagonists ; Genes, vif ; Genetic Variation ; Humans ; Pharmacogenetics ; Receptors, Adrenergic ; Receptors, Corticotropin-Releasing Hormone ; Receptors, Leukotriene

Myasthenia gravis is believed to be an autoimmune disease involving morphologic and electrophysiologic disturbances of motor end plates brought about by circulating antibodies against acetylcholine receptors. Its treatment includes the use of steroids, anticholinesterase, immunosuppression and plasmapheresis. Plasmapheresis, in particular, is used either as a stand-alone temporary measure for its often dramatic, though short-lived, effect, or as an adjunctive treatment. Plasmapheresis is considered to be essential not only in preventing and treating myasthenic crisis but in preoperative management of myasthenia gravis, usually before thymectomy. the authors here report a case of myasthenia gravis that underwent preoperative plasmapheresis followed by the use of atracurium for muscle relaxation during anesthesia for thymectomy.
Anesthesia* ; Antibodies ; Atracurium ; Autoimmune Diseases ; Immunosuppression ; Muscle Relaxation ; Myasthenia Gravis* ; Plasmapheresis* ; Receptors, Cholinergic ; Steroids ; Thymectomy

Organophosphate (OP) pesticides are the most common source of human toxicity globally, causing high mortality and morbidity despite the availability of atropine as a specific antidote and oximes to reactivate acetylcholinesterase. The primary toxicity mechanism is inhibition of acetylcholinesterase (AchE), resulting in accumulation of the neurotransmitter, acetylcholine, and abnormal stimulation of acetylcholine receptors. Thus, the symptoms (muscarinic, nicotinic, and central nervous system) result from cholinergic overactivity because of AchE inhibition. OP can also cause rhabdomyolysis, pancreatitis, parotitis, and hepatitis. OP therapy includes decontamination, supportive therapy, and the use of specific antidotes such as atropine and oximes. However, there has been a paucity of controlled trials in humans. Here we evaluated the literature for advances in therapeutic strategies for acute OP poisoning over the last 10 years.
Acetylcholine ; Acetylcholinesterase ; Antidotes ; Atropine ; Decontamination ; Hepatitis ; Humans ; Neurotransmitter Agents ; Oximes ; Pancreatitis ; Parotitis ; Pesticides ; Receptors, Cholinergic ; Rhabdomyolysis