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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Ishii R, Shinozuka K, Kunitomo M, Hashimoto T, Takeuchi K

Department of Pharmacology, Meiji College of Pharmacy, Tokyo, Japan.

Clin Exp Pharmacol Physiol. 1996 May;23(5):395-6. doi: 10.1111/j.1440-1681.1996.tb02747.x.

The release of endogenous noradrenaline (NA) and adenyl purine (ATP, ADP, AMP and adenosine) from the rabbit ear artery, evoked by electrical stimulation (ES; 16 Hz), was examined. 2. ES evoked a significant release of NA and purine; the ratio of the amount of total purine released to NA released was approximately 180 on a molar base. 3. ES-evoked purine release was significantly reduced by the denudation of the endothelium and abolished by the alpha 1-adrenoceptor antagonist, prazosin (1 mumol/L). 4. ES-evoked NA release was significantly reduced by a P1-purinoceptor antagonist, 8-sulfophenyl theophylline (8SPT). Purine release was slightly reduced by 8SPT. 5. These results suggest that endogenous NA released by ES results in the release of a large amount of purine, which may, in turn, increase the release of NA by acting on prejunctional purinoceptors on sympathetic nerve terminals.

研究了电刺激（ES；16赫兹）诱发兔耳动脉释放内源性去甲肾上腺素（NA）和腺嘌呤（ATP、ADP、AMP和腺苷）的情况。2. 电刺激诱发了显著的去甲肾上腺素和嘌呤释放；以摩尔为基础，释放的总嘌呤量与去甲肾上腺素释放量的比值约为180。3. 内皮剥脱显著降低了电刺激诱发的嘌呤释放，α1肾上腺素能受体拮抗剂哌唑嗪（1微摩尔/升）可消除该释放。4. P1嘌呤受体拮抗剂8-磺苯基茶碱（8SPT）显著降低了电刺激诱发的去甲肾上腺素释放。8SPT使嘌呤释放略有减少。5. 这些结果表明，电刺激释放的内源性去甲肾上腺素导致大量嘌呤释放，而嘌呤反过来可能通过作用于交感神经末梢的突触前嘌呤受体增加去甲肾上腺素的释放。

Ishii R, Shinozuka K, Kunitomo M, Hashimoto T, Takeuchi K

Department of Pharmacology, Meiji College of Pharmacy, Tokyo, Japan.

Clin Exp Pharmacol Physiol. 1996 May;23(5):395-6. doi: 10.1111/j.1440-1681.1996.tb02747.x.

The release of endogenous noradrenaline (NA) and adenyl purine (ATP, ADP, AMP and adenosine) from the rabbit ear artery, evoked by electrical stimulation (ES; 16 Hz), was examined. 2. ES evoked a significant release of NA and purine; the ratio of the amount of total purine released to NA released was approximately 180 on a molar base. 3. ES-evoked purine release was significantly reduced by the denudation of the endothelium and abolished by the alpha 1-adrenoceptor antagonist, prazosin (1 mumol/L). 4. ES-evoked NA release was significantly reduced by a P1-purinoceptor antagonist, 8-sulfophenyl theophylline (8SPT). Purine release was slightly reduced by 8SPT. 5. These results suggest that endogenous NA released by ES results in the release of a large amount of purine, which may, in turn, increase the release of NA by acting on prejunctional purinoceptors on sympathetic nerve terminals.

研究了电刺激（ES；16赫兹）诱发兔耳动脉释放内源性去甲肾上腺素（NA）和腺嘌呤（ATP、ADP、AMP和腺苷）的情况。2. 电刺激诱发了显著的去甲肾上腺素和嘌呤释放；以摩尔为基础，释放的总嘌呤量与去甲肾上腺素释放量的比值约为180。3. 内皮剥脱显著降低了电刺激诱发的嘌呤释放，α1肾上腺素能受体拮抗剂哌唑嗪（1微摩尔/升）可消除该释放。4. P1嘌呤受体拮抗剂8-磺苯基茶碱（8SPT）显著降低了电刺激诱发的去甲肾上腺素释放。8SPT使嘌呤释放略有减少。5. 这些结果表明，电刺激释放的内源性去甲肾上腺素导致大量嘌呤释放，而嘌呤反过来可能通过作用于交感神经末梢的突触前嘌呤受体增加去甲肾上腺素的释放。