product name Atropine sulfate monohydrate
Description: Atropine sulfate monohydrate is a competitive antagonist for the muscarinic acetylcholine receptor, it is used to decrease the production of saliva and secretions of the airway prior to surgery. Atropine exerts the pharmacological effects by binding to muscarinic acetylcholine receptors. Atropine, the orthosteric antagonist, has been reported to compete with [3H]-NMS for all muscarinic subtypes with a potency consistent with the high affinities at the mAChR subtypes. The Ki values are 1.27±0.36nM, 3.24±1.16nM, 2.21±0.53nM, 0.77±0.43nM and 2.84±0.84nM, respectively.
References: Vis Neurosci. 2000 Mar-Apr;17(2):165-76; Neurosci Lett. 2003 Jul 17;345(2):97-100.
694.83
Formula
2(C17H23NO3).H2O.H2SO4
CAS No.
5908-99-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 139 mg/mL (200 mM)
Water: 139 mg/mL (200 mM)
Ethanol: 139 mg/mL (200 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390620
| In Vitro |
In vitro activity: Atropine increases the release of the neurotransmitter dopamine into the superfusate in vitro at 100-500 mM and into the vitreous in vivo at 250 mg. Atropine induces spreading depression (SD) in the in vitro preparation. Atropine reduces the ERG b- and d-wave, leads to damped oscillations of RPE potentials, and reverses the ERG c-wave. Atropine suppresses myopia only at doses at which severe nonspecific side effects are observed in the retina. Kinase Assay: Atropine increases the release of the neurotransmitter dopamine into the superfusate in vitro at 100-500 mM and into the vitreous in vivo at 250 mg. Atropine induces spreading depression (SD) in the in vitro preparation. Atropine reduces the ERG b- and d-wave, leads to damped oscillations of RPE potentials, and reverses the ERG c-wave. Atropine suppresses myopia only at doses at which severe nonspecific side effects are observed in the retina. Cell Assay: |
|---|---|
| In Vivo | Atropine (1.0 mg/kg, i.p.), but not methylatropine (1.0 mg/kg, i.p.), prevents the enhancement of retention induced by both doses of the anticholinesterase when given immediately after training in mice. Atropine administration effectively prevents bradycardia and second-degree heart block but induces pulsus alternans and hypertension in dogs. Atropine has no effect on handling-induced acetylcholine output in the presence of 10 nM neostigmine, but causes greater and longer increases in the presence of 100 nM and 1000 nM neostigmine in rats. Atropine not only blocks the rapid eye movement (REM) sleep increases induced by CGS but it also tends to decrease REM sleep compared to atropine preceding saline in rats. Atropine decreases the time to exhaustion by 67% in intact rats and by 96.2% in adrenodemedullated (ADM) and also reduces the exercise-induced pituitary prolactin (PRL) release in both intact (50%) and ADM rats (90%). |
| Animal model | |
| Formulation & Dosage | |
| References | Vis Neurosci. 2000 Mar-Apr;17(2):165-76; Neurosci Lett. 2003 Jul 17;345(2):97-100. |
Related Posts
product name Atropine sulfate monohydrate
Description: Atropine sulfate monohydrate is a competitive antagonist for the muscarinic acetylcholine receptor, it is used to decrease the production of saliva and secretions of the airway prior to surgery. Atropine exerts the pharmacological effects by binding to muscarinic acetylcholine receptors. Atropine, the orthosteric antagonist, has been reported to compete with [3H]-NMS for all muscarinic subtypes with a potency consistent with the high affinities at the mAChR subtypes. The Ki values are 1.27±0.36nM, 3.24±1.16nM, 2.21±0.53nM, 0.77±0.43nM and 2.84±0.84nM, respectively.
References: Vis Neurosci. 2000 Mar-Apr;17(2):165-76; Neurosci Lett. 2003 Jul 17;345(2):97-100.
694.83
Formula
2(C17H23NO3).H2O.H2SO4
CAS No.
5908-99-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 139 mg/mL (200 mM)
Water: 139 mg/mL (200 mM)
Ethanol: 139 mg/mL (200 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19390620
| In Vitro |
In vitro activity: Atropine increases the release of the neurotransmitter dopamine into the superfusate in vitro at 100-500 mM and into the vitreous in vivo at 250 mg. Atropine induces spreading depression (SD) in the in vitro preparation. Atropine reduces the ERG b- and d-wave, leads to damped oscillations of RPE potentials, and reverses the ERG c-wave. Atropine suppresses myopia only at doses at which severe nonspecific side effects are observed in the retina. Kinase Assay: Atropine increases the release of the neurotransmitter dopamine into the superfusate in vitro at 100-500 mM and into the vitreous in vivo at 250 mg. Atropine induces spreading depression (SD) in the in vitro preparation. Atropine reduces the ERG b- and d-wave, leads to damped oscillations of RPE potentials, and reverses the ERG c-wave. Atropine suppresses myopia only at doses at which severe nonspecific side effects are observed in the retina. Cell Assay: |
|---|---|
| In Vivo | Atropine (1.0 mg/kg, i.p.), but not methylatropine (1.0 mg/kg, i.p.), prevents the enhancement of retention induced by both doses of the anticholinesterase when given immediately after training in mice. Atropine administration effectively prevents bradycardia and second-degree heart block but induces pulsus alternans and hypertension in dogs. Atropine has no effect on handling-induced acetylcholine output in the presence of 10 nM neostigmine, but causes greater and longer increases in the presence of 100 nM and 1000 nM neostigmine in rats. Atropine not only blocks the rapid eye movement (REM) sleep increases induced by CGS but it also tends to decrease REM sleep compared to atropine preceding saline in rats. Atropine decreases the time to exhaustion by 67% in intact rats and by 96.2% in adrenodemedullated (ADM) and also reduces the exercise-induced pituitary prolactin (PRL) release in both intact (50%) and ADM rats (90%). |
| Animal model | |
| Formulation & Dosage | |
| References | Vis Neurosci. 2000 Mar-Apr;17(2):165-76; Neurosci Lett. 2003 Jul 17;345(2):97-100. |