Dipyridamole (tablet): Difference between revisions
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==Category== | ==Category== | ||
Cardiovascular Drugs: | Cardiovascular Drugs:Antiplatelet drugs | ||
==US Brand Names== | ==US Brand Names== | ||
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'''| [[Dipyridamole indications and usage|Indications and Usage]]''' | '''| [[Dipyridamole indications and usage|Indications and Usage]]''' | ||
'''| [[Dipyridamole dosage and administration|Dosage and Administration]]''' | '''| [[Dipyridamole dosage and administration|Dosage and Administration]]''' | ||
'''| [[Dipyridamole contraindications|Contraindications]]''' | '''| [[Dipyridamole contraindications|Contraindications]]''' | ||
'''| [[Dipyridamole warnings and precautions|Warnings and Precautions]]''' | '''| [[Dipyridamole warnings and precautions|Warnings and Precautions]]''' | ||
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'''| [[Dipyridamole clinical pharmacology|Clinical Pharmacology]]''' | '''| [[Dipyridamole clinical pharmacology|Clinical Pharmacology]]''' | ||
'''| [[Dipyridamole nonclinical toxicology|Nonclinical Toxicology]]''' | '''| [[Dipyridamole nonclinical toxicology|Nonclinical Toxicology]]''' | ||
'''| [[Dipyridamole how supplied storage and handling|How Supplied/Storage and Handling]]''' | '''| [[Dipyridamole how supplied storage and handling|How Supplied/Storage and Handling]]''' | ||
'''| [[Dipyridamole labels and packages|Labels and Packages]]''' | '''| [[Dipyridamole labels and packages|Labels and Packages]]''' | ||
==Mechanism of Action== | ==Mechanism of Action== | ||
Dipyridamole inhibits the uptake of [[adenosin]]e into platelets, endothelial cells and erythrocytes in vitro and in vivo; the inhibition occurs in a dose-dependent manner at therapeutic concentrations (0.5–1.9 μg/mL). This inhibition results in an increase in local concentrations of [[adenosin]]e which acts on the platelet A2-receptor thereby stimulating platelet adenylate cyclase and increasing platelet cyclic-3',5'-[[adenosin]]e monophosphate (cAMP) levels. Via this mechanism, platelet aggregation is inhibited in response to various stimuli such as platelet activating factor (PAF), collagen and [[adenosin]]e diphosphate (ADP). | |||
Dipyridamole inhibits phosphodiesterase (PDE) in various tissues. While the inhibition of cAMP-PDE is weak, therapeutic levels of dipyridamole inhibit cyclic-3',5'-guanosine monophosphate-PDE (cGMP-PDE), thereby augmenting the increase in cGMP produced by EDRF (endothelium-derived relaxing factor, now identified as nitric oxide). | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{Antithrombotics}} | |||
[[Category:Antiplatelet drugs]] | |||
[[Category:Cardiovascular Drugs]] | [[Category:Cardiovascular Drugs]] | ||
[[Category:Drugs]] | [[Category:Drugs]] | ||
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Revision as of 03:24, 7 February 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sheng Shi, M.D. [2]
For patient information about Dipyridamole, click here
Synonyms / Brand Names: PERSANTINE®
Overview
Category
Cardiovascular Drugs:Antiplatelet drugs
US Brand Names
FDA Package Insert
| Indications and Usage | Dosage and Administration | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | How Supplied/Storage and Handling | Labels and Packages
Mechanism of Action
Dipyridamole inhibits the uptake of adenosine into platelets, endothelial cells and erythrocytes in vitro and in vivo; the inhibition occurs in a dose-dependent manner at therapeutic concentrations (0.5–1.9 μg/mL). This inhibition results in an increase in local concentrations of adenosine which acts on the platelet A2-receptor thereby stimulating platelet adenylate cyclase and increasing platelet cyclic-3',5'-adenosine monophosphate (cAMP) levels. Via this mechanism, platelet aggregation is inhibited in response to various stimuli such as platelet activating factor (PAF), collagen and adenosine diphosphate (ADP).
Dipyridamole inhibits phosphodiesterase (PDE) in various tissues. While the inhibition of cAMP-PDE is weak, therapeutic levels of dipyridamole inhibit cyclic-3',5'-guanosine monophosphate-PDE (cGMP-PDE), thereby augmenting the increase in cGMP produced by EDRF (endothelium-derived relaxing factor, now identified as nitric oxide).