Adenosine Receptor Subtypes and Cardioprotection in Cardiac Myocyte and Transgenic Models

Author(s):  
G. Paul Matherne ◽  
John P. Headrick ◽  
Bruce T. Liang
1997 ◽  
Vol 357 (1) ◽  
pp. 1-9 ◽  
Author(s):  
K.-N. Klotz ◽  
J. Hessling ◽  
J. Hegler ◽  
C. Owman ◽  
B. Kull ◽  
...  

1993 ◽  
Vol 113 (2) ◽  
pp. 257-261 ◽  
Author(s):  
M. R. Zarrindast ◽  
M. Modabber ◽  
M. Sabetkasai

1997 ◽  
Vol 272 (1) ◽  
pp. H25-H34 ◽  
Author(s):  
T. Abe ◽  
D. A. Morgan ◽  
D. D. Gutterman

Adenosine plays an important role in postischemic dysfunction of cardiac sympathetic nerves because exogenously infused adenosine produces and adenosine deaminase prevents “neural stunning.” We examined whether adenosine acts via a specific receptor mechanism to produce neural stunning. Anesthetized dogs were treated with propranolol to attenuate increases in coronary flow due to adrenergic stimulation of myocardial metabolism. A 15-min occlusion of the left anterior descending coronary artery (LAD) attenuated subsequent LAD coronary vasoconstriction to bilateral sympathetic stimulation during reperfusion by 75% (P < 0.05). Coronary infusion of the adenosine-receptor antagonist 8-p-sulfophenyltheophylline (nonspecific), 8-cyclopentyl-1,3-dipropylxanthine (A1 specific), or 3,7-dimethyl-1-propagylxanthine (A2 specific) during LAD occlusion prevented the attenuation of sympathetic coronary constriction. In separate experiments, either the specific adenosine agonist N6-cyclopentyl-adenosine (A1 specific) or CGS-21680 (A2 specific) or a combination of both agonists was infused into the LAD for 15 min. Neither agonist alone attenuated subsequent sympathetic coronary constriction. In contrast, 15 min after the combined administration of both agonists, sympathetic vasoconstriction was reduced. We conclude that adenosine is capable of attenuating neurogenic coronary constriction through a receptor-mediated mechanism. Activation of more than one receptor subtype is necessary to produce neural stunning.


2010 ◽  
Vol 480 (3) ◽  
pp. 182-185 ◽  
Author(s):  
Hyung Gon Lee ◽  
Woong Mo Kim ◽  
Jeong Il Choi ◽  
Myung Ha Yoon

ChemInform ◽  
2004 ◽  
Vol 35 (40) ◽  
Author(s):  
Wolfgang Guba ◽  
Matthias Nettekoven ◽  
Bernd Puellmann ◽  
Claus Riemer ◽  
Sebastien Schmitt

Pharmacology ◽  
2006 ◽  
Vol 78 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Myung Ha Yoon ◽  
Hong Beom Bae ◽  
Jeong Il Choi ◽  
Seok Jai Kim ◽  
Sung Tae Chung ◽  
...  

2019 ◽  
Vol 20 (21) ◽  
pp. 5475 ◽  
Author(s):  
Nina Wolska ◽  
Marcin Rozalski

Adenosine receptors are a subfamily of highly-conserved G-protein coupled receptors. They are found in the membranes of various human cells and play many physiological functions. Blood platelets express two (A2A and A2B) of the four known adenosine receptor subtypes (A1, A2A, A2B, and A3). Agonization of these receptors results in an enhanced intracellular cAMP and the inhibition of platelet activation and aggregation. Therefore, adenosine receptors A2A and A2B could be targets for anti-platelet therapy, especially under circumstances when classic therapy based on antagonizing the purinergic receptor P2Y12 is insufficient or problematic. Apart from adenosine, there is a group of synthetic, selective, longer-lasting agonists of A2A and A2B receptors reported in the literature. This group includes agonists with good selectivity for A2A or A2B receptors, as well as non-selective compounds that activate more than one type of adenosine receptor. Chemically, most A2A and A2B adenosine receptor agonists are adenosine analogues, with either adenine or ribose substituted by single or multiple foreign substituents. However, a group of non-adenosine derivative agonists has also been described. This review aims to systematically describe known agonists of A2A and A2B receptors and review the available literature data on their effects on platelet function.


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