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大鼠尾动脉内源性三磷酸腺苷的释放。

Release of endogenous ATP from rat caudal artery.

作者信息

Westfall D P, Sedaa K, Bjur R A

出版信息

Blood Vessels. 1987;24(3):125-7. doi: 10.1159/000158684.

Abstract

Electrical field stimulation of the rat caudal artery (0.5-ms pulses at 8 Hz for 3 min) results in the release of norepinephrine (quantified by HPLC-electrochemical detection) and adenyl purines including ATP, ADP and AMP (quantified by HPLC-fluorescence detection). The amount of ATP released from the tissue exceeded the amount of norepinephrine. Because postjunctional alpha 1-adrenoceptor stimulation with methoxamine also causes release of ATP, both neuronal and extraneuronal sites may contribute to the overflow of ATP. Results with the alpha 1-adrenoceptor antagonist prazosin lend support to this notion. Prazosin (10(-6) M) completely blocked the release of ATP by methoxamine but only partially reduced the release of ATP by field stimulation.

摘要

对大鼠尾动脉进行电场刺激(8赫兹,0.5毫秒脉冲,持续3分钟)会导致去甲肾上腺素释放(通过高效液相色谱 - 电化学检测定量)以及包括ATP、ADP和AMP在内的腺苷嘌呤释放(通过高效液相色谱 - 荧光检测定量)。从组织中释放的ATP量超过了去甲肾上腺素的量。由于用甲氧明对节后α1 - 肾上腺素能受体进行刺激也会导致ATP释放,所以神经元和非神经元部位都可能导致ATP溢出。α1 - 肾上腺素能受体拮抗剂哌唑嗪的实验结果支持了这一观点。哌唑嗪(10^(-6) M)完全阻断了甲氧明引起的ATP释放,但仅部分降低了电场刺激引起的ATP释放。

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