5 In the presence of a cyclic AMP phosphodiesterase inhibitor, the effects of CGS 21680 on cyclic AMP accumulation and 5-HT release were enhanced to levels similar to those elicited by 10 gM NECA. In the absence of phosphodiesterase inhibition, CGS 21680 did not antagonise the effects of NECA. Furthermore, endogenous adenosine did not contribute to the effects of CGS 21680 when phosphodiesterase was inhibited. 6 We conclude that an A2a adenosine receptor appears to be involved in the NECAelicited increases in cyclic AMP levels and inhibition of 5-HT release in human platelets. However, the difference in efficacy between NECA and the A2a-selective agonist CGS 21680, observed in the absence but not the presence of a phosphodiesterase inhibitor, suggests that other mechanisms must underlie this differential effect.
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