1 The effect of adenosine and some adenosine analogues on the isolated thoracic aorta from rats was compared with the effect of adenosine 5'-triphosphate (ATP) and adenosine 5'-diphosphate (ADP). 2 Both ATP and adenosine analogues caused relaxation of the noradrenaline (30 nM)-contracted thoracic aorta.3 The order of potency for adenosine analogues was 5'-(N-ethyl) carboxamidoadenosine (NECA) > L-N6-phenylisopropyladenosine (L-PIA), adenosine 5'-monophosphate (AMP), adenosine indicating the presence of adenosine A2 receptors. 4 Removal of the endothelium or prior treatment with haemoglobin (10 pM) attenuated relaxant responses to both ATP and NECA, attenuation being greater for ATP than NECA. 5 8-Phenyltheophylline (1OgM) reduced relaxant responses to NECA but not to ATP in the intact tissue. 6 These results provide evidence that there are two components to relaxation of the rat thoracic aorta induced by purinoceptor agonists. The first is an endothelium-dependent mechanism involving release of endothelium-derived relaxant factor (EDRF) and the second is due to a direct effect on smooth muscle.
1The effects of dopamine on vasoconstrictor responses to field stimulation of sympathetic nerves and to exogenous noradrenaline were studied in the isolated ear artery of the rabbit. Responses to sympathetic nerve stimulation were depressed, initially, by infusions of dopamine (0.5 to 1 gM), but the responses partially recovered in the continued presence of dopamine. Responses to noradrenaline were unchanged at the start of the dopamine infusions but were enhanced as the infusions continued and also after cessation of the infusion.
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