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  • Title: P1(A2/Ra)-purinoceptors may mediate the stimulatory effect of adenosine and adenosine analogs on acid formation in isolated rabbit parietal cells.
    Author: Ainz LF, Salgado C, Gandarias JM, Gomez R, Vallejo A, Gil-Rodrigo CE.
    Journal: Pharmacol Res; 1993; 27(4):319-34. PubMed ID: 8103595.
    Abstract:
    The effects of adenosine (ADO) and its analogs 2-chloroadenosine (2CADO) and 5'-N-ethyl-carboxamido adenosine (NECA) on acid production, as measured by the [14C]-aminopyrine (AP) accumulation method, were studied in rabbit gastric parietal cells prepared by enzymatic dispersion and enriched by counterflow elutriation. ADO (1 microM to 1 mM), 2CADO (1 microM to 1 mM) and NECA (0.1 microM to 100 microM) caused significant concentration-related increases on AP uptake by resting parietal cells. The order of potency was NECA >> 2CADO > or = ADO. Histamine and dibutyryl-cAMP (db-cAMP), known secretagogues, stimulated AP accumulation. In both, histamine- and db-cAMP-stimulated parietal cells, ADO, 2CADO and NECA at the above concentration ranges induced concentration-related increases of the respective AP accumulation raised-rates. The rank order of potency in both stimulated conditions was: NECA > 2CADO >> ADO. Cimetidine, a well known H2 histamine receptor antagonist, at concentration of 100 microM caused potent inhibition of histamine-stimulated AP accumulation without affecting the stimulatory responses to db-cAMP. The increases of AP accumulation elicited by NECA, the most potent purine tested, in both resting and histamine- or db-cAMP-stimulated parietal cells were not significantly modified by cimetidine 100 microM. Theophylline (0.1 microM to 10 microM), a non-specific P1-purinoceptor antagonist, caused significant inhibition of the NECA responses in both resting and histamine-stimulated parietal cells. The concentration order of potency of theophylline was: 0.1 microM > 1 microM > 10 microM. These results suggest that there are P1(A2/Ra)-purinoceptors on rabbit parietal cells which mediate the stimulatory effects of adenosine and analogs on gastric acid production.
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