Sperlágh B, Illes P, Gerevich Z, Köfalvi A
Department of Pharmacology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest.
Neurochem Res. 2001 Sep;26(8-9):951-7. doi: 10.1023/a:1012336601854.
The temperature-dependence of ATP release and contraction response evoked by different agonists were investigated in superfused guinea-pig vas deferens. Alpha-adrenoceptor agonists, i.e. noradrenaline (300 microM), and alpha-methyl-noradrenaline (300 microM), increased the basal ATP outflow, measured by the luciferin-luciferase assay, and induced biphasic contractile response. Cooling the bath temperature to 12 degrees C almost completely inhibited ATP release and twitch contraction evoked by alpha-adrenoceptor agonists, whereas the phasic contraction remained unaffected. In contrast, twitch contraction and subsequent ATP release induced by beta,gamma-methylene-ATP, a selective P2 receptor agonist (100 microM), was not reduced by low temperature. The ectoATPase activity, measured by HPLC technique was not significantly different at 37 degrees C and 12 degrees C. Nifedipine (1 microM), the voltage sensitive Ca2+ channel blocker eliminated beta,gamma-methylene-ATP evoked twitch contraction but not ATP release. In conclusion, alpha-adrenoceptor and P2 receptor agonists utilize distinct mechanisms to elicit ATP release and contraction: alpha-adrenoceptor-mediated ATP release and contraction is temperature-dependent, indicating the involvement of a carrier-mediated process in it, whereas P2x purinoceptor evoked ATP release and twitch is mediated by a different mechanism.
在灌流的豚鼠输精管中，研究了不同激动剂诱发的ATP释放和收缩反应的温度依赖性。α-肾上腺素能受体激动剂，即去甲肾上腺素（300微摩尔）和α-甲基去甲肾上腺素（300微摩尔），通过荧光素-荧光素酶测定法测量，增加了基础ATP流出，并诱导了双相收缩反应。将浴温冷却至12℃几乎完全抑制了α-肾上腺素能受体激动剂诱发的ATP释放和抽搐收缩，而相性收缩不受影响。相反，选择性P2受体激动剂β，γ-亚甲基-ATP（100微摩尔）诱导的抽搐收缩和随后的ATP释放不受低温影响。通过HPLC技术测量的胞外ATP酶活性在37℃和12℃时无显著差异。电压敏感钙通道阻滞剂硝苯地平（1微摩尔）消除了β，γ-亚甲基-ATP诱发的抽搐收缩，但不影响ATP释放。总之，α-肾上腺素能受体和P2受体激动剂利用不同机制引发ATP释放和收缩：α-肾上腺素能受体介导的ATP释放和收缩是温度依赖性的，表明其中涉及载体介导的过程，而P2x嘌呤受体诱发的ATP释放和抽搐是由不同机制介导的。
