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高钾通过内源性去甲肾上腺素诱发兔肺动脉释放ATP。

High potassium-evoked release of ATP from rabbit pulmonary artery via endogenous noradrenaline.

作者信息

Takeuchi K, Ishii R, Shinozuka K, Hashimoto T

机构信息

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

出版信息

Gen Pharmacol. 1995 Oct;26(6):1385-90. doi: 10.1016/0306-3623(94)00302-4.

Abstract
  1. High potassium 30 mM and noradrenaline at 10 microM significantly evoked the release of ATP and produced remarkable vasoconstriction in the rabbit pulmonary artery. 2. Phentolamine and prazosin at 0.1 microM inhibited ATP release but not vasoconstriction by 30 mM potassium. 3. 30 mM potassium significantly evoked the release of noradrenaline. 4. There was a significant positive correlation between the amounts of release of total purines, sum of ATP, ADP, AMP and adenosine, and noradrenaline evoked by 30 mM potassium. 5. 30 mM potassium-evoked ATP release was significantly reduced by denudation of endothelium.
摘要
  1. 30毫摩尔的高钾和10微摩尔的去甲肾上腺素能显著诱发兔肺动脉中ATP的释放,并产生明显的血管收缩。2. 0.1微摩尔的酚妥拉明和哌唑嗪可抑制ATP释放,但不能抑制30毫摩尔钾引起的血管收缩。3. 30毫摩尔的钾能显著诱发去甲肾上腺素的释放。4. 30毫摩尔钾诱发的总嘌呤释放量、ATP、ADP、AMP和腺苷的总量与去甲肾上腺素释放量之间存在显著正相关。5. 内皮剥脱可显著降低30毫摩尔钾诱发的ATP释放。

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