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  • Title: Adenosine mediates nitric-oxide-independent renal vasodilation by activation of A2A receptors.
    Author: Rump LC, Jabbari-T J, von Kügelgen I, Oberhauser V.
    Journal: J Hypertens; 1999 Dec; 17(12 Pt 2):1987-93. PubMed ID: 10703900.
    Abstract:
    OBJECTIVE: Adenosine dilates rabbit renal arteries by an endothelium-dependent, nitric oxide (NO)- and prostaglandin-independent mechanism. The aim was to identify the responsible P1-purinoceptor subtype and to investigate the involvement of K+-channels. METHODS: Rabbit renal arteries were perfused with medium containing indomethacin (10 micromol/l). After preconstriction with noradrenaline (0.4 micromol/l), changes in vessel diameter by P1-purinoceptor agonists were measured with a photoelectric device. The P1-receptor subtype was characterised by selective antagonists. RESULTS: Adenosine caused concentration-dependent dilation (EC50 approximately 7 micromol/l). The mRNA for A1, A2A and A3 receptors were demonstrated by reverse transcription-polymerase chain reaction from total RNA of renal arteries. The agonists CPCA (A2) and CGS21680 (A2A) dilated renal arteries (EC50 approximately 0.1 micromol/l), and CPA (A1) was ineffective. As demonstrated by experiments using two arteries in sequence, CPCA induced release of an endothelium-derived relaxing factor. NO synthase inhibition by NG-nitro-L-arginine methyl ester (L-NAME) had no effect on CPCA-induced dilation. The concentration-response curves of adenosine, CPCA and CGS21680 were shifted to the right by the A2A antagonist ZM241385 (1 micromol/l), but not by the A1 and A3 antagonists DPCPX (1 micromol/l) and MRS1220 (1 micromol/l). Iberiotoxin (0.1 micromol/l), a blocker of Ca2+-activated K+-channels, slightly shifted the dose- response curve of CPCA. Arteries preconstricted by KCl showed dilation to CPCA, but not to acetylcholine chloride (ACh). CONCLUSION: Adenosine induces dilation of rabbit renal arteries through activation of A2A receptors. This effect depends on the release of an endothelium-derived relaxing factor, which is not NO. Dilation by ACh in the presence of L-NAME is likely to be mediated by K+ as an endothelium-derived relaxing factor. However, in the A2A-receptor-induced dilation of rabbit renal arteries, K+ does not play this role, suggesting the involvement of a further soluble factor in the receptor-induced dilatory function of the endothelium.
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