Adenosine

   

                 Package Insert     

            Adenosine is a  purine nucleoside that forms from the breakdown of dephosphorylated adenosine triphosphate by the  enzyme, 5'-nucleotidase. Adenosine produces vasodilation  and increases coronary blood flow. Adenosine binds to adenosine type 2A (A2A) receptors, which are coupled to the Gs-protein. Activation of this G-protein stimulates adenylyl cyclase, increases cAMP and causes protein kinase activation. This stimulates KATP channels, which hyperpolarizes the smooth muscle, causing relaxation. Increased cAMP also causes smooth muscle relaxation by inhibiting myosin light chain kinase, which leads to decreased myosin phosphorylation and a decrease in contractile force. There is also evidence that adenosine inhibits calcium entry into the cell through L-type calcium channels. Since calcium regulates smooth muscle contraction, reduced intracellular calcium causes relaxation. Adenosine has a very short half-life. In human blood, its half-life is less than 10 seconds. There are two important metabolic fates for adenosine. Most importantly, adenosine is rapidly transported into red blood cells (and other cell types) where it is rapidly deaminated by adenosine deaminase to inosine, which is further broken down to hypoxanthine, xanthine and uric acid, which is excreted by the kidneys. Adenosine deamination also occurs in the plasma, but at a lower rate than that which occurs within cells. Dipyridamole is a vasodilator drug that blocks adenosine uptake by cells, thereby reducing the metabolism of extracellular adenosine.

            Patients can experience flushing and headache, both of which are related to vasodilation. Adenosine can produce rapid arterial hypotension and AV block, however, these are reversed shortly after ceasing the infusion of adenosine.

 References:

1 Gupta NC, Esterbrooks DJ, Hilleman DE, Mohiuddin SM. Comparison of adenosine and exercise thallium-201 single-photon emission computed tomography (SPECT) myocardial perfusion imaging. The GE SPECT Multicenter Adenosine Study Group. J Am Coll Cardiol. 1992 Feb;19(2):248-57.

2 Amanullah AM, Berman DS, Hachamovitch R, Kiat H, Kang X, Friedman JD. Identification of severe or extensive coronary artery disease in women byadenosine technetium-99m sestamibi SPECT.Am J Cardiol. 1997 Jul 15;80(2):132-7.

3 Klabunde, Richard E. Cardiovascular Pharmacology Concepts.(http://www.cvpharmacology.com/index.html).

Home     Index    Myocardial  Spect Thallium   Myocardial  Spect Mibi  Myocardial Pharmacologic Intervention