Pronounced direct inhibitory action mediated by adenosine A1 receptor and pertussis toxin-sensitive G protein on the ferret ventricular contraction

1993 ◽  
Vol 348 (3) ◽  
Author(s):  
M. Endoh ◽  
M. Takanashi ◽  
I. Norota ◽  
Y Kawabata ◽  
T. Asano
Keyword(s):  
G Protein ◽  
Pertussis Toxin ◽  
Inhibitory Action ◽  
Adenosine A1 Receptor ◽  
Ventricular Contraction ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine attenuates calcium paradox injury: role of adenosine A1 receptor

1995 ◽  
Vol 268 (4) ◽  
pp. C838-C845 ◽  
Author(s):  
J. Suleiman ◽  
M. Ashraf
Keyword(s):  
Pertussis Toxin ◽  
Receptor Activation ◽  
Isolated Rat Heart ◽  
Adenosine A1 Receptor ◽  
Mechanical Activity ◽  
Dependent Manner ◽  
Protective Effects ◽  
Lactate Dehydrogenase Release ◽  
Adenosine A1 ◽  
A1 Receptor

The present study was conducted to test the hypothesis that adenosine attenuates the Ca2+ paradox (PD) injury via stimulation of adenosine A1 receptors linked to Gi proteins in the isolated rat heart. Treatment of adenosine reduced maximum lactate dehydrogenase release and ATP loss compared with regular Ca2+ PD. Recovery of mechanical activity after Ca2+ repletion was observed only in heart treated with adenosine before and during the Ca2+ PD. Significant preservation of myocytes was observed in adenosine-treated hearts compared with the regular Ca2+ PD. Adenosine exerted its effects in a dose-dependent manner, being maximum at 100 microM. The protective effects were mediated by adenosine A1 receptor activation since the adenosine A1 receptor agonist N6-phenylisopropyladenosine provided protection similar to adenosine-treated heart and was blocked by A1 receptor antagonist and pertussis toxin. This study suggests that protection by adenosine against the lethal injury of the Ca2+ PD is mediated by adenosine A1 receptor and a pertussis toxin-sensitive inhibiting G protein.

Adenosine A1 receptor-dependent G-protein activity in the rat brain during prolonged wakefulness

Neuroreport ◽  
2004 ◽  
Vol 15 (13) ◽  
pp. 2133-2137 ◽  
Author(s):  
Lauri O. Alanko ◽  
Jarmo T. Laitinen ◽  
Dag Stenberg ◽  
Tarja Porkka-Heiskanen
Keyword(s):  
Rat Brain ◽  
G Protein ◽  
Adenosine A1 Receptor ◽  
Protein Activity ◽  
Adenosine A1 ◽  
A1 Receptor

scholarly journals P109Opposite actions of atrial adenosine A1 receptor on G protein-coupled inwardly-rectifying potassium (GIRK/Kir3.1/3.4) and small Ca2+-activated K+ outward (KCa2/SK) currents

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S18.5-S19
Author(s):  
B Braganca ◽  
N Oliveira-Monteiro ◽  
S Nogueira-Marques ◽  
F Ferreirinha ◽  
PA Lima ◽  
...  
Keyword(s):  
G Protein ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Inwardly Rectifying ◽  
G Protein Coupled

scholarly journals The Signaling Pathways Involved in the Anticonvulsive Effects of the Adenosine A1 Receptor

2020 ◽  
Vol 22 (1) ◽  
pp. 320
Author(s):  
Jeroen Spanoghe ◽  
Lars E. Larsen ◽  
Erine Craey ◽  
Simona Manzella ◽  
Annelies Van Dycke ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
G Protein ◽  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Neuronal Inhibition ◽  
Adenosine A1 ◽  
Mitogen Activated Protein ◽  
A1 Receptor ◽  
G Protein Coupled

Adenosine acts as an endogenous anticonvulsant and seizure terminator in the brain. Many of its anticonvulsive effects are mediated through the activation of the adenosine A1 receptor, a G protein-coupled receptor with a wide array of targets. Activating A1 receptors is an effective approach to suppress seizures. This review gives an overview of the neuronal targets of the adenosine A1 receptor focusing in particular on signaling pathways resulting in neuronal inhibition. These include direct interactions of G protein subunits, the adenyl cyclase pathway and the phospholipase C pathway, which all mediate neuronal hyperpolarization and suppression of synaptic transmission. Additionally, the contribution of the guanyl cyclase and mitogen-activated protein kinase cascades to the seizure-suppressing effects of A1 receptor activation are discussed. This review ends with the cautionary note that chronic activation of the A1 receptor might have detrimental effects, which will need to be avoided when pursuing A1 receptor-based epilepsy therapies.

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