Release of norepinephrine and dopamine from brain vesicular preparations: Effects of adenosine analogues

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Abstract
1. Adenosine analogues inhibit calcium-dependent K+-evoked release of [3H]norepinephrine from guinea pig cerebral cortical and hippocampal vesicular preparations. Inhibition requires high concentrations (100µM) of the adenosine analogues and is abolished in the presence of high concentrations (2 mM) of calcium ions. The inhibitory effect of 2-chloroadenosine is blocked by theophylline. The structure activity profile (N6-d-phenylisopropyladenosine ≥N6-l-phenylisopropyladenosine ≥ 2-chloroadenosine >N6-cyclohexyladenosine, adenosine 5′-cyclopropylcar-boxamide) is not that expected of either A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 2. Calcium-dependent K+-evoked release of [3H]dopamine from guinea pig striatal vesicular preparations is inhibited by apomorphine. However, only 2-chloroadenoine causes an inhibition of K+-evoked release of [3H]dopamine. Other adenosine analogues such asd- andl-phenylisopropyladenosine and adenosine 5′-cyclopropylcar-boxamide cause a facilitation of K+-evoked release. The facilitation is abolished or reduced in the presence of high concentrations (2 mM) of calcium ions. The sites of action of adenosine analogues do not appear to have structural requirements identical to those expected of A1 (high-affinity) or A2 (low-affinity) adenosine receptors. 3. The results indicate that adenosine analogues can have either inhibitory or facilitory effects on K+-evoked release of catecholamines from central synaptic terminals.

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