Stojanov I, Proctor K G
Department of Physiology, University of Tennessee Health Science Center, Memphis.
J Pharmacol Exp Ther. 1990 Jun;253(3):1083-9.
The A1 and A2 adenosine receptor agonists (5'-(N-ethylcarboxamido)-adenosine, 2-chloroadenosine, adenosine (ADO) and N6-cyclohexyladenosine) were topically applied to 30- to 60-microns arterioles in the s.c. microcirculation of hamsters at different skin temperatures. Vasoconstrictor responses evoked by nanomolar concentrations of ADO and N6-cyclohexyladenosine were enhanced when local skin temperature (Ts) was increased, but unchanged when Ts was decreased. All these responses were antagonized by 8-phenyltheophylline, which suggests that temperature-sensitive vasoconstrictions were mediated by A1 receptors. In contrast, norepinephrine (10(-7) M) caused vasoconstrictions that were not enhanced at high Ts and were markedly reduced at low Ts, while angiotensin II (10(-8) M) caused vasoconstrictions that were temperature-insensitive. Vasodilator responses evoked by micromolar concentrations of ADO, 2-chloroadenosine and 5'-(N-ethylcarboxamido)-adenosine were temperature-insensitive. All these responses were antagonized by 8-phenyltheophylline, except those mediated by 10(-6) to 10(-4) M ADO, which can be explained by simple override of the receptor blockade. Thus, A1, but not A2, receptors show temperature-dependent actions in vivo, which suggests that temperature sensitivity could be an additional criterion for classification of ADO receptors.
将A1和A2腺苷受体激动剂（5'-（N-乙基甲酰胺基）-腺苷、2-氯腺苷、腺苷（ADO）和N6-环己基腺苷）局部应用于不同皮肤温度下仓鼠皮下微循环中30至60微米的小动脉。当局部皮肤温度（Ts）升高时，纳摩尔浓度的ADO和N6-环己基腺苷引起的血管收缩反应增强，但当Ts降低时则无变化。所有这些反应均被8-苯基茶碱拮抗，这表明温度敏感的血管收缩是由A1受体介导的。相比之下，去甲肾上腺素（10^-7 M）引起的血管收缩在高Ts时未增强，在低Ts时明显减弱，而血管紧张素II（10^-8 M）引起的血管收缩对温度不敏感。微摩尔浓度的ADO、2-氯腺苷和5'-（N-乙基甲酰胺基）-腺苷引起的血管舒张反应对温度不敏感。所有这些反应均被8-苯基茶碱拮抗，但10^-6至10^-4 M ADO介导的反应除外，这可以通过受体阻断的简单超越来解释。因此，A1受体而非A2受体在体内表现出温度依赖性作用，这表明温度敏感性可能是ADO受体分类的另一个标准。
