Adenosine: Difference between revisions
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==Mechanism of Action== | ==Mechanism of Action== | ||
When administered intravenously, adenosine causes transient [[heart block]] in the [[atrioventricular node|atrioventricular (AV) node]]. This is mediated via the [[Adenosine A receptor|A<sub>1</sub> receptor]], inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilation of the "normal" segments of arteries, i.e. where the [[endothelium]] is not separated from the tunica media by [[atherosclerotic plaque]]. This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments. | |||
==References== | ==References== |
Revision as of 17:33, 11 March 2014
Adenosine |
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ADENOCARD®, ADENOSCAN® 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 |
Clinical Studies |
How Supplied/Storage and Handling |
Labels and Packages |
Clinical Trials on Adenosine |
ClinicalTrials.gov |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, M.D. [2]
Synonyms / Brand Names: ADENOCARD®, ADENOSCAN®
Overview
Adenosine (ADO) is a purine nucleoside comprising a molecule of adenine attached to a ribose sugar molecule (ribofuranose) moiety via a β-N9-glycosidic bond.Adenosine plays an important role in biochemical processes, such as energy transfer — as adenosine triphosphate (ATP) and adenosine diphosphate (ADP) — as well as in signal transduction as cyclic adenosine monophosphate, cAMP. It is also an inhibitory neurotransmitter, believed to play a role in promoting sleep and suppressing arousal. Adenosine also plays a role in regulation of blood flow to various organs through vasodilation.[1][2][3]
Category
FDA Package Insert[4]
| Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages
Mechanism of Action
When administered intravenously, adenosine causes transient heart block in the atrioventricular (AV) node. This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K+ flux. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilation of the "normal" segments of arteries, i.e. where the endothelium is not separated from the tunica media by atherosclerotic plaque. This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments.
References
- ↑ Sato, A; Terata, K; Miura, H; Toyama, K; Loberiza FR, Jr; Hatoum, OA; Saito, T; Sakuma, I; Gutterman, DD (April 2005). "Mechanism of vasodilation to adenosine in coronary arterioles from patients with heart disease". American journal of physiology. Heart and circulatory physiology. 288 (4): H1633–40. doi:10.1152/ajpheart.00575.2004. PMID 15772334.
- ↑ Costa, F; Biaggioni, I (May 1998). "Role of nitric oxide in adenosine-induced vasodilation in humans". Hypertension. 31 (5): 1061–4. doi:10.1161/01.HYP.31.5.1061. PMID 9576114.
- ↑ Morgan, JM; McCormack, DG; Griffiths, MJ; Morgan, CJ; Barnes, PJ; Evans, TW (September 1991). "Adenosine as a vasodilator in primary pulmonary hypertension". Circulation. 84 (3): 1145–9. doi:10.1161/01.CIR.84.3.1145. PMID 1884445.
- ↑ "ADENOCARD (ADENOSINE) SOLUTION [ASTELLAS PHARMA US, INC.]".