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muscarine/hipersensitivitas
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Enhanced responses to muscarine in rats treated chronically with atropine.
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Rats were treated for 14 or 30 days with 10 mg/kg sc atropine (AT) daily. 24 h after the last dose of At, 50 micrograms of muscarine (MU) was injected intracerebroventricularly (ivtr.). Long-term atropinization enhanced the behavior induced by MU. These data support our previous suggestion that
Histamine and acetylcholine regulation of sympathetic nerve activity in guinea-pig nasal mucosa.
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The regulating effects of histamine and acetylcholine (Ach) in norepinephrine (NE) transmission in nasal mucosa were investigated by analyzing 3H-NE release from isolated guinea-pig tissues. In addition, localization of the histamine H1 receptor and the muscarinic acetylcholine receptor on the
Activation of the SPHK/S1P signalling pathway is coupled to muscarinic receptor-dependent regulation of peripheral airways.
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BACKGROUND
In peripheral airways, acetylcholine induces contraction via activation of muscarinic M2-and M3-receptor subtypes (M2R and M3R). Cholinergic hypersensitivity is associated with chronic obstructive pulmonary disease and asthma, and therefore the identification of muscarinic signaling
[Pharmacology of astemizole (Hismanal) a non-sedating H1 antihistaminic].
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In the compound 48/80 lethality test in rats, which is based on the specific activation of mast cells, astemizole was found to be a potent, long-acting and orally very effective inhibitor of anaphylactoid shock. In comparison to other histamine-H1 antagonists, astemizole was remarkably free of
Cholinergic stimulation attenuates the IL-4 induced expression of E-selectin and vascular endothelial growth factor by equine pulmonary artery endothelial cells.
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The endothelium plays a critical role in regulating leukocyte recruitment and migration during inflammation. Recent studies provide evidence that acetylcholine (ACh) and other cholinergic mediators block endothelial cells activation and leukocyte recruitment during inflammation. We thus postulated
RE1-silencing transcription factor controls the acute-to-chronic neuropathic pain transition and Chrm2 receptor gene expression in primary sensory neurons.
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Neuropathic pain is associated with persistent changes in gene expression in primary sensory neurons, but the underlying epigenetic mechanisms that cause these changes remain unclear. The muscarinic cholinergic receptors (mAChRs), particularly the M2 subtype (encoded by the cholinergic receptor
Role of muscarinic receptor subtypes in the constriction of peripheral airways: studies on receptor-deficient mice.
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In the airways, increases in cholinergic nerve activity and cholinergic hypersensitivity are associated with chronic obstructive pulmonary disease and asthma. However, the contribution of individual muscarinic acetylcholine receptor subtypes to the constriction of smaller intrapulmonary airways that
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