Collis M G, Brown C M
Eur J Pharmacol. 1983 Dec 9;96(1-2):61-9. doi: 10.1016/0014-2999(83)90529-0.
The purpose of this study was to determine whether the adenosine receptor that mediates relaxation of the noradrenaline-contracted guinea-pig aorta is of the A1 or A2 subtype. 5'-N-ethylcarboxamide adenosine (NECA) and 5'-N-cyclopropylcarboxamide adenosine (NCPCA) were about 100 times more potent as relaxants of the aorta than L-N6-phenylisopropyladenosine (L-PIA) and N6-cyclohexyladenosine. L-PIA was 3 times more potent than D-PIA. These relaxations were not altered by the purine transport inhibitor dipyridamole, but were attenuated by the cell surface adenosine receptor antagonist 8-phenyltheophylline. Adenosine and 2-chloroadenosine differed from NECA and NCPCA since they evoked greater maximal relaxations and their submaximal responses were less sensitive to blockade by 8-phenyltheophylline. These differences were abolished by dipyridamole which indicates that they were due to an intracellular action of adenosine and 2-chloroadenosine. The intracellular 'P-site' agonist, 9-beta-D-xylofuranosyladenine evoked small relaxations that were attenuated by dipyridamole but were unaffected by 8-phenyltheophylline. These results indicate that adenosine can relax the aorta via interactions with a cell surface A2 receptor and with an intracellular site.
本研究的目的是确定介导去甲肾上腺素收缩的豚鼠主动脉舒张的腺苷受体是A1还是A2亚型。5'-N-乙基甲酰胺腺苷（NECA）和5'-N-环丙基甲酰胺腺苷（NCPCA）作为主动脉舒张剂的效力比L-N6-苯异丙基腺苷（L-PIA）和N6-环己基腺苷强约100倍。L-PIA的效力比D-PIA强3倍。这些舒张作用不受嘌呤转运抑制剂双嘧达莫的影响，但被细胞表面腺苷受体拮抗剂8-苯基茶碱减弱。腺苷和2-氯腺苷与NECA和NCPCA不同，因为它们引起更大的最大舒张，并且它们的次最大反应对8-苯基茶碱的阻断不太敏感。双嘧达莫消除了这些差异，这表明它们是由于腺苷和2-氯腺苷的细胞内作用。细胞内“P位点”激动剂9-β-D-呋喃木糖基腺嘌呤引起小的舒张，被双嘧达莫减弱，但不受8-苯基茶碱影响。这些结果表明，腺苷可通过与细胞表面A2受体和细胞内位点相互作用使主动脉舒张。
