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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

Lewis C J, Surprenant A, Evans R J

Department of Cell Physiology & Pharmacology, University of Leicester, UK.

Br J Pharmacol. 1998 Aug;124(7):1463-6. doi: 10.1038/sj.bjp.0702001.

P2X receptor activation by alpha,beta-meATP evoked inward currents in acutely dissociated rat mesenteric artery smooth muscle cells and contractions of whole artery rings. 2. The selective P2X1 and P2X3 receptor antagonist TNP-ATP inhibited P2X receptor mediated inward currents in response to 3 microM alpha,beta-meATP (an approximately EC90 concentration) with an IC50 of approximately 2 nM. This provides further evidence that the P2X receptor underlying membrane depolarisation associated with P2X receptor activation can be accounted for by the expression of P2X1 receptors. 3. TNP-ATP inhibited alpha,beta-meATP induced contractions with an IC50 of approximately 30 microM and had non-specific effects on smooth muscle contraction. 4. The reduced potency of TNP-ATP in whole tissue experiments probably reflects the breakdown of TNP-ATP by nucleotidases. Thus, TNP-ATP is of limited use in whole tissue experiments as a P2X receptor antagonist.

α,β-甲硫腺苷三磷酸（α,β-meATP）激活P2X受体可在急性分离的大鼠肠系膜动脉平滑肌细胞中诱发内向电流，并使整个动脉环收缩。2. 选择性P2X1和P2X3受体拮抗剂三硝基苯腺苷三磷酸（TNP-ATP）抑制了P2X受体介导的内向电流，该电流是对3微摩尔α,β-meATP（约为EC90浓度）的反应，其半数抑制浓度（IC50）约为2纳摩尔。这进一步证明，与P2X受体激活相关的膜去极化所涉及的P2X受体可由P2X1受体的表达来解释。3. TNP-ATP抑制α,β-meATP诱导的收缩，IC50约为30微摩尔，且对平滑肌收缩有非特异性作用。4. 在全组织实验中TNP-ATP效力降低可能反映了核苷酸酶对TNP-ATP的分解。因此，TNP-ATP作为P2X受体拮抗剂在全组织实验中的用途有限。

Lewis C J, Surprenant A, Evans R J

Department of Cell Physiology & Pharmacology, University of Leicester, UK.

Br J Pharmacol. 1998 Aug;124(7):1463-6. doi: 10.1038/sj.bjp.0702001.

P2X receptor activation by alpha,beta-meATP evoked inward currents in acutely dissociated rat mesenteric artery smooth muscle cells and contractions of whole artery rings. 2. The selective P2X1 and P2X3 receptor antagonist TNP-ATP inhibited P2X receptor mediated inward currents in response to 3 microM alpha,beta-meATP (an approximately EC90 concentration) with an IC50 of approximately 2 nM. This provides further evidence that the P2X receptor underlying membrane depolarisation associated with P2X receptor activation can be accounted for by the expression of P2X1 receptors. 3. TNP-ATP inhibited alpha,beta-meATP induced contractions with an IC50 of approximately 30 microM and had non-specific effects on smooth muscle contraction. 4. The reduced potency of TNP-ATP in whole tissue experiments probably reflects the breakdown of TNP-ATP by nucleotidases. Thus, TNP-ATP is of limited use in whole tissue experiments as a P2X receptor antagonist.

α,β-甲硫腺苷三磷酸（α,β-meATP）激活P2X受体可在急性分离的大鼠肠系膜动脉平滑肌细胞中诱发内向电流，并使整个动脉环收缩。2. 选择性P2X1和P2X3受体拮抗剂三硝基苯腺苷三磷酸（TNP-ATP）抑制了P2X受体介导的内向电流，该电流是对3微摩尔α,β-meATP（约为EC90浓度）的反应，其半数抑制浓度（IC50）约为2纳摩尔。这进一步证明，与P2X受体激活相关的膜去极化所涉及的P2X受体可由P2X1受体的表达来解释。3. TNP-ATP抑制α,β-meATP诱导的收缩，IC50约为30微摩尔，且对平滑肌收缩有非特异性作用。4. 在全组织实验中TNP-ATP效力降低可能反映了核苷酸酶对TNP-ATP的分解。因此，TNP-ATP作为P2X受体拮抗剂在全组织实验中的用途有限。