The cardiac depressant effects of purines in rat atria are mediated by a receptor that does not conform to the traditional A1/A2 classification system.
Challenges A1/A2 classification in rat atria; leaves open novel receptor targets in human cardiac physiology.
The effects of a series of adenosine derivatives were examined on the catecholamine-stimulated electrically-driven rat left atrium in vitro. All the purines tested reduced the positive inotropic action of isoprenaline, 0.1 microM, with the potency order: L-N6-phenlylisopropyladenosine (L-PIA) greater than 5'-N-ethylcarboxamide adenosine (NECA) greater than D-PIA greater than 2-chloroadenosine greater than adenosine. Dipyridamole did not change the IC50 of adenosine. The adenosine deaminase inhibitor, 2'deoxycoformycin, produced a small but nonsignificant shift to the left of the adenosine concentration-response curve. The cardiac depressant effects of these purines were reversed by theophylline and the IC50 values were unchanged in the presence of atropine or in atria taken from reserpine-treated rats. It is concluded that the purine receptor mediating these effects should not be classified on the A1/A2 system. The relationship between functionally characterized purine receptors and those originally defined as modulating adenylate cyclase is discussed.
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Hughes et al. (1983) studied this question.
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