Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In diabetic rats, intestinal mucin secretion is unusually high compared with that in normal rats. These studies demonstrate that mucin synthesis is also increased in the diabetic intestine. alpha- and beta-adrenergic agonists or antagonists did not affect mucin output in either normal or diabetic animals, suggesting that altered release in diabetes was not due to goblet cells responding abnormally to adrenergic agents. The cholinergic agonist bethanechol caused a dose-dependent and atropine-sensitive increase in mucin secretion from the normal intestine but had no effect on mucin release from diabetic tissue. Atropine alone did not reduce mucin secretion from the diabetic intestine to levels found in normal tissue. Cholera toxin caused an approximately fivefold increase in mucin output from normal rats but had no effect on mucin secretion from diabetic animals. Thus, goblet cell responses to cholinergic stimulation and cholera toxin in the diabetic intestine are markedly impaired. However, loss of cholinergic control does not appear to be responsible for altered baseline mucin secretion in diabetes.
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PMID:Intestinal mucin secretion in streptozotocin-diabetic rats: lack of response to cholinergic stimulation and cholera toxin. 168 17

Pieces of ferret trachea and human bronchi were mounted in Ussing chambers and given [35S]sulphate as a radiolabelled precursor of mucous glycoproteins (mucins). The output of 35S bound to macromolecules was studied as an index of mucin secretion. In the ferret trachea, electrical field stimulation increased the rate of mucin secretion. Tetrodotoxin (10(-7) M or 10(-6) M) abolished this effect. Pilocarpine (25 microM) stimulated the output of mucins from human bronchus. Atropine (10(-5) M) abolished this effect. Electrical field stimulation of human bronchus stimulated mucin secretion. Tetrodotoxin (10(-6) M) abolished this effect. Field stimulation in the presence of either atropine (10(-5) M) or atropine with l-propranolol (10(-5) M) and phentolamine (10(-5) M) caused no stimulation of mucin secretion rate. Some bronchi were treated with noradrenaline (10(-5) M) for 1 h to allow the adrenergic nerves to take up transmitter. Even in these, atropine prevented the effect of field stimulation. We conclude that activity in cholinergic nerves can stimulate mucin secretion in the bronchi in man. Our results provide no evidence that the adrenergic nerves or non-adrenergic, non-cholinergic nerves have a direct action on bronchial secretory cells in man.
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PMID:Nervous control of mucin secretion into human bronchi. 403 17

The widely used muscarinic receptor ligand [3H]quinuclidinyl benzilate ([3H]QNB) was found to bind in a site-specific but artifactual manner to rat intestinal mucus, obscuring specific binding to muscarinic receptors on intestinal epithelial cells. Atropine inhibited [3H]QNB binding to mucus with an apparent IC50 of 2.1 x 10(-7) M, compared to an IC50 of 1.4 x 10(-8) M obtained with a homogenate of intestinal epithelial cells. Unlabeled QNB also inhibited binding of [3H]QNB to mucus but the apparent IC50 (4 x 10(-7) M) was about 300-fold greater than the IC50 determined with a control tissue, heart muscle (IC50, 1.2 x 10(-9) M). [3H]QNB binding was saturable over the concentration range of 1-7 nM in the heart, with an apparent KD of 0.76 nM. As expected from the high IC50 for QNB in the mucus binding experiments, binding to mucus was not saturable over the 1-15 nM concentration range. Based on pH profiles and temperature dependency of binding, it seems unlikely that mucin, the primary component of mucus, was responsible for [3H]QNB binding to the mucus. The findings have implications for studies which involve binding of [3H]QNB in particular and other ligands in general to mucus-secreting epithelial tissues.
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PMID:Binding of [3H]quinuclidinyl benzilate to intestinal mucus. An artifact in identification of epithelial cell muscarinic receptors. 706 20

Brompheniramine and chlorpheniramine have anticholinergic activities, but the relative potency of these effects has not been well defined. The anticholinergic properties of brompheniramine, chlorpheniramine, and atropine were assessed in an in vitro model of human nasal mucosal glandular secretion. Methacholine was used as a cholinergic agonist to stimulate glandular secretion of 7F10-mucin. These drugs (0.01-1000 microM) or vehicle (saline) were added to explant cultures with and without 100 microM methacholine. 7F10-mucin concentrations were measured in culture supernatants after 2-hour incubations. The effective dose reducing methacholine-induced secretion (ED50) was determined. ED50 was 0.25 microM for atropine, 4.10 microM for brompheniramine, and 4.63 microM for chlorpheniramine. None of the anticholinergic drugs changed spontaneous glandular exocytosis. Brompheniramine and chlorpheniramine are equipotent anticholinergic agents in human nasal mucosa in vitro. Atropine was 16 to 19 times more potent.
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PMID:Anticholinergic properties of brompheniramine, chlorpheniramine, and atropine in human nasal mucosa in vitro. 957 32