Disease relevance of ADORA1

• Activation of the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning hypoxia and simulate preconditioning, with a maximal effect at 100 nM [1].
• The inhibitory adenosine A1 receptor pathway was first inactivated by pertussis toxin treatment of the cultures, and the effects of adenosine agonists and antagonists on the heart cell contractile amplitude, measured via an opticovideo motion detection system, and on the modulation of cAMP level were determined [2].

High impact information on ADORA1

• Homologous sensitisation of embryonic chick atrial myocytes to adenosine: mediation by adenosine A1 receptor and guanine nucleotide binding protein [3].
• RESULTS: Removal of adenosine from the culture medium with adenosine deaminase resulted in an enhanced ability of the adenosine A1 receptor agonist R-N6-(2-phenylisopropyl)-adenosine to exert a direct, negative inotropic effect and to inhibit isoprenaline stimulated adenylyl cyclase activity [3].
• Binding of the antagonist radioligand [3H]-8-cyclopentyl-1,3-dipropylxanthine in membranes from myocytes pre-exposed to adenosine deaminase showed a 70% increase in the adenosine A1 receptor density and a 54% increase in the proportion of the high affinity adenosine A1 receptor: control 33(5)%, n = 5, versus sensitised 49(3)%, n = 5, p < 0.01 [3].
• METHODS: The ability of adenosine A1 receptor to mediate inhibition of adenylyl cyclase activity and myocyte contractility was determined in atrial myocytes cultured from 14 d chick embryos [3].
• 6. Adenosine A1 receptor agonists significantly inhibit the K(+)-stimulated release of [3H]-acetylcholine from the rabbit retina, suggesting that endogenous adenosine may modulate the light-evoked or tonic release of ACh [4].

Anatomical context of ADORA1

• Under conditions in which the myocytes were sensitised to the effects of A1 agonist, changes in the levels of adenosine A1 receptor and pertussis toxin sensitive G proteins were determined and correlated with alterations in the adenylyl cyclase activity and contractile responses of the myocyte to the A1 agonist [3].

References