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1. The adenosine receptors mediating relaxation of porcine isolated left anterior descending coronary arteries (LAD) and the effects of the level and type of preconstriction on the responses to adenosine analogues were examined in the present study.

2. Relaxation responses to the non-selective adenosine receptor agonist N-ethylcarboxamidoadenosine (NECA) were endothelium independent. N-Ethylcarboxamidoadenosine, GR 79236 (A1 receptor selective) and 8-cyclopentyl-1,3-dipropylxanthine (CGS 21680) (A2A receptor selective) produced full relaxation in LAD precontracted to 50% of the response to potassium depolarization with the thromboxane receptor agonist U46619. The order of potency was CGS 21680 = NECA > GR 79236, consistent with that defining the A2A receptor subtype.

3. 3,7-Dimethyl-1-propargylxanthine (DMPX; A2 receptor selective) competitively antagonized NECA and CGS 21680 with pKB values of 4.95±0.09 and 5.06±0.22, respectively. The A1 receptor selective antagonist 1,3-[3H]-dipropyl-8-cyclopentylxanthine (DPCPX) had no effect on NECA relaxation, even in the presence of DMPX.

4. The sensitivity to relaxation by NECA was dependent on the precontracting agent. Arteries precontracted with endothelin (ET)-1 were most sensitive to NECA, U46619-precontracted arteries were intermediate and KCl-precontracted arteries were least sensitive.

5. The potency of NECA was reduced when the preconstriction level was increased from 50 to 90% of maximum in U46619-precontracted arteries (pEC50 7.94±0.12 and 7.35±0.04, respectively) and, in KCl-precontracted arteries, both the potency and maximum effect of NECA were reduced when the preconstriction level increased from 50 to 80% of maximum (pEC50 7.52±0.13 and 6.91±0.26, respectively; maximum responses 82.5±10.2 and 23.9±3.6%, respectively, of the preconstricted tone). Relaxation responses to NECA were independent of the level of precontraction in ET-1-precontracted arteries.

6. In porcine LAD, relaxation responses to adenosine analogues were endothelium independent and were mediated via A2A adenosine receptors. Responses to NECA were dependent on both the level and type of preconstriction.

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