Burka J F
Can J Physiol Pharmacol. 1986 Mar;64(3):225-30. doi: 10.1139/y86-035.
The modulatory effects of adenosine and selected derivatives were examined on antigen and arachidonic acid (AA) induced contractions of indomethacin-treated tracheal spirals and lung parenchymal strips from actively sensitized guinea pigs. Adenosine (up to 2 X 10(-4) M) had no effect on antigen-induced contractions, but inhibited AA-induced contractions by 30-40% if added 30 min prior to challenge. The weak effect of adenosine suggests that endogenous adenosine may only have a limited modulatory role in allergic bronchospasm. 2-Chloroadenosine (10(-6)-10(-4) M) dose-dependently inhibited antigen- and AA-induced contractions of trachea, but was considerably less effective on parenchyma. The substituted adenosine derivatives, R-phenylisopropyladenosine (R-PIA) and 5'-(N-ethylcarboxamido)-adenosine (NECA), and the adenosine transport inhibitor, 6-[p-nitrobenzyl)thio]-9-beta-D-ribofuranosyl purine, were also active as modulators, but their activity was relatively weak and varied with the stimulus and the tissue. An order of potency for R-PIA, NECA, and 2-chloroadenosine could not be determined and 8-phenyltheophylline (10(-5) M) was not an effective inhibitor of the effects of adenosine or the adenosine derivatives. This suggests that adenosine and its derivatives may modulate cells through mechanisms other than activation of conventional A1 and A2 receptors. A lack of specificity for the adenosine derivatives must also be considered.
研究了腺苷及其某些衍生物对经消炎痛处理的、来自主动致敏豚鼠的气管螺旋条和肺实质条在抗原和花生四烯酸（AA）诱导下收缩的调节作用。腺苷（浓度高达2×10⁻⁴ M）对抗原诱导的收缩无影响，但在激发前30分钟添加时，可使AA诱导的收缩抑制30 - 40%。腺苷的作用较弱，提示内源性腺苷在过敏性支气管痉挛中可能仅具有有限的调节作用。2 - 氯腺苷（10⁻⁶ - 10⁻⁴ M）剂量依赖性地抑制气管对抗原和AA诱导的收缩，但对实质条的作用明显较弱。取代腺苷衍生物R - 苯异丙基腺苷（R - PIA）和5' - （N - 乙基羧酰胺） - 腺苷（NECA）以及腺苷转运抑制剂6 - [对硝基苄基）硫代] - 9 - β - D - 呋喃核糖基嘌呤也作为调节剂有活性，但其活性相对较弱，且随刺激和组织的不同而变化。无法确定R - PIA、NECA和2 - 氯腺苷的效价顺序，且8 - 苯基茶碱（10⁻⁵ M）不是腺苷或腺苷衍生物作用的有效抑制剂。这表明腺苷及其衍生物可能通过激活传统A1和A2受体以外的机制调节细胞。还必须考虑腺苷衍生物缺乏特异性这一因素。
