Disease relevance of Tropin

• Peripheral cholinergic blockade with methylatropine did not alter the leukotriene hypotension [1].
• Intraperitoneal (i.p.) injection of methylatropine (0.01 mmol/100 g of body weight), which does not cross the blood-brain barrier, also did not affect the basal levels of ANP 30 min after i.p. injection [2].
• Even stronger correlations were observed between changes in these parameters after methylatropine and vagal tone, particularly in the atrial fibrillation group (correlation coefficients of .89, .87, .72, and .90, respectively) [3].
• The hypothermia in AChE mutant mice was fully rescued by a peripheral injection of both ivermectin, which increases nicotinic receptor currents, and methyl-atropine, a muscarinic antagonist [4].
• Peripheral methylatropine blocked bradycardia and unmasked tachycardia, which implies concurrent autonomic discharges on early trials [5].

Psychiatry related information on Tropin

• Passive avoidance learning was significantly impaired by atropine (5 mg/kg, IP) or scopolamine (0.5 mg/kg), but not by methyl-atropine (5 mg/kg) or methyl-scopolamine (0.5 mg/kg), from postnatal day 15 on [6].
• Intraperitoneal injection of atropine, but not methylatropine, caused dose-related stereotyped behavior in the rat and this effect was antagonized by intracaudate injection of triperidol in a dose-related manner [7].

High impact information on Tropin

• OXO-induced LCGU increases were not influenced by methylatropine (1 mg/kg, s.c.) but were antagonized completely by scopolamine (2.5 mg/kg, i.p.). Scopolamine reduced LCGU in layer IV of the auditory cortex and in the retrosplenial cortex [8].
• beta-Cell tropin, the pituitary peptide ACTH22-39, is a potent insulin secretagogue and stimulates lipogenesis in adipose tissue in rodents [9].
• Underlying autonomic mechanisms were then assessed by repeating the baroreflex tests after either cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol [10].
• Both vagal and sympathetic function were assessed through intravenous injections of methylatropine and propranolol [11].
• Underlying autonomic mechanisms were then examined by repetition of baroreceptor reflex tests after cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol [12].

Chemical compound and disease context of Tropin

• Ethanol (1 g/kg i.v) did not influence the residual reflex bradycardia after methyl-atropine, but significantly decreased the residual reflex bradycardia after propranolol [13].
• Reflex bradycardia was elicited by phenylephrine-induced hypertension in conscious and pentobarbital anesthetized (PA) rats before and after sympathetic blockade with the beta-1 receptor antagonist atenolol or parasympathetic blockade with the peripherally acting muscarinic receptor antagonist methyl-atropine [14].
• The bradycardia was abolished by the muscarinic acetylcholine receptor antagonist methylatropine [15].
• The administration of methylatropine (0.3 mg/kg i.v.) to sham-operated rats only prevented the bradycardia induced by neostigmine (1 microgram i.c.v.), the pressor response was not affected [16].
• Reflex bradycardia induced by all doses of phenylephrine was almost totally blocked blocked following methyl-atropine treatment [17].

Biological context of Tropin

• In rats pretreated with atenolol or in rats with the cervical section of spinal cord and the low level of heart rate increased with an isoprenaline infusion, the decrease in heart rate produced by pergolide was abolished by domperidone, methylatropine or idazoxan [18].
• However, methylatropine did not affect either the vasoconstriction or the vasodilatation [19].
• Atropine and methylatropine (10 mumol kg-1 i.p.) increased the LD50 value of BR 401, given i.v., 75- to 100-fold [20].
• The compound reduced blood pressure and spontaneous sympathetic outflow in anesthetized cats after blockade of peripheral muscarinic receptors with methylatropine [21].
• Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone [22].

Anatomical context of Tropin

• To investigate a possible role of TSH in the regulation of its own receptor, a sensitive assay of [125I]TSH tropin binding to rat thyroid membranes was used [23].
• Measurements were performed after administration of saline as vehicle or during manipulation of the autonomic nervous system by infusion of metoprolol, methyl-atropine and hexamethonium [24].
• The pKB values for pirenzepine on the stomach (6.67) and the trachea (6.87) were not significantly different suggesting that pirenzepine behaves more like N-methylatropine in terms of expressed affinity [25].
• Thus, 3H-QNB binding in hypothalamus of young and adult rats was increased (31% and 17%) after chronic IVT methylatropine and decreased (20% and 15%) after IVT oxotremorine [26].
• In contrast, parasympathetic nervous system blockade with methyl-atropine produced relatively less inhibition of baroreflex gain in the PA rat compared with the conscious rat [14].

Associations of Tropin with other chemical compounds

• The involvement of postsynaptic alpha 2-adrenergic receptors in the adrenergic constriction of the capacitance vessels was studied in anesthetized, spontaneously breathing dogs under ganglionic blockade (hexamethonium, 10 mg/kg + 10 mg/kg/hr; methylatropine, 0.5 mg/kg) [27].
• Prior acute subdiaphragmatic vagotomy or i.p. pre-injection with methylatropine (10(-8) mol) completely prevented the neostigmine-induced rise in plasma insulin concentration [28].
• Beta-cell tropin- and glucose-induced hypersecretion of insulin and amylin from perfused fatty rat pancreas [29].
• The changes of heart rate in response to i.v. administration of methylatropine (0.5 mg/kg) and/or propranolol (2 mg/Kg) or practolol (2.5 mg/Kg) were studied in conscious trained dogs [30].
• Administration of the mixed muscarinic/nicotinic receptor agonist carbachol caused a decrease, whereas administration of the muscarinic receptor antagonist methyl-atropine caused an increase in the output of acetylcholine in both the hippocampus and the medial septal area [31].

Gene context of Tropin

• Methylatropine further accelerated tachycardia and diminished the enhanced BRS in the IR group [32].
• beta-cell tropin, a peptide of the pituitary pars intermedia which stimulates insulin release [33].
• The administration of oxotremorine together with methylatropine to rats produces a dose-dependent increase of adrenal dopamine-beta-hydroxylase (DBH) activity [34].
• The method was employed to compare plasma Beta-cell tropin concentrations between lean and genetically obese (ob/ob) mice and between lean and genetically obese (fa/fa) Zucker rats [35].
• In addition, methylatropine, at a dose of 0.5 nmol, significantly reduced the increase in diastolic pressure produced by the TRH agonist [36].

Analytical, diagnostic and therapeutic context of Tropin

• But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine [2].
• The molecular weight of tropin T kinase as determined by gel filtration exceeds 500 000 [37].
• Pretreatment of rats with either bilateral vagotomy or i. v. methylatropine (1 mg/kg) did not modify significantly the hypotensive and bradycardic responses to EOMV [38].
• Neither methylatropine pretreatment nor adrenalectomy prevented the response to TRH injected into the nha, suggesting that activation of the cardiac sympathetic nerves may mediate TRH actions in this region [39].
• The results show that the hyperglycemic response to hemorrhage was decreased by either methylatropine (H-MA) treatment or bilateral carotid receptor denervation (10.3+/-0.4 mM, control, n=15 vs. 7.7+/-0.2 mM, H-MA, n=12, and 7.6+/-0.3 mM, H-CD, n=5, p<0.01) [40].

References