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P2U嘌呤受体和P2Y嘌呤受体对金黄仓鼠离体肠系膜动脉床内皮依赖性血管舒张的相对贡献。

Relative contribution of P2U- and P2Y-purinoceptors to endothelium-dependent vasodilatation in the golden hamster isolated mesenteric arterial bed.

作者信息

Ralevic V, Burnstock G

机构信息

Department of Anatomy and Developmental Biology, University College London.

出版信息

Br J Pharmacol. 1996 Apr;117(8):1797-802. doi: 10.1111/j.1476-5381.1996.tb15357.x.

Abstract
  1. P2-purinoceptors were characterized pharmacologically in the constantly perfused isolated mesenteric arterial vascular bed of the golden hamster. Vasoconstrictor and vasodilator responses to the nucleotides ATP, ADP, 2 methylthio ATP (2MeSATP), alpha,beta-methylene ATP (alpha,beta-meATP) and uridine 5'-triphosphate (UTP) and a role for ATP in sympathetic constriction were examined. 2. At basal tone nucleotides elicited dose-dependent vasoconstriction with an observed rank order of potency of alpha,beta-meATP >> 2MeSATP > ATP = ADP > UTP (based on the doses required to elicit constrictor responses of 25 mmHg). Adenosine had no vasoconstrictor action at doses up to 5 mumol. After application of a single dose (0.5 mumol) of alpha,beta-meATP preparations were desensitized to constriction by subsequent application of nucleotides. 3. Electrical field stimulation (4-64 Hz, 90 V, 1 ms, 30 s) elicited frequency-dependent constrictions which were abolished by guanethidine (5 microM) and by prazosin (1 microM). 4. The non-selective P2-purinoceptor antagonist suramin (100 microM) did not significantly affect vasoconstrictor responses to ATP. The P2X-selective purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 3 microM), virtually abolished responses to ATP. When the endothelium was removed vasoconstrictor responses to ATP and noradrenaline were augmented. 5. In preparations with tone raised with methoxamine (10-80 microM) nucleotides elicited vasodilatation with an observed potency order of ATP = UTP > ADP >> adenosine. 2MeSATP had relatively minor vasodilator effects and at the highest dose tested (50 nmol) elicited only vasoconstriction. alpha,beta-meATP did not elicit vasodilatation but produced further constriction of the raised tone preparation. At the highest doses of ATP and ADP (0.5 microM) responses were biphasic with vasoconstriction preceding vasodilatation. After removal of the endothelium, with the exception of adenosine, vasodilator responses to purines and to UTP were abolished; vasoconstriction to ATP, ADP, UTP and 2MeSATP was evident at the highest doses. 6. Suramin (100 microM) inhibited vasodilatation to both ATP and UTP and abolished responses to 2MeSATP. PPADS (3 microM) inhibited relaxation to 2MeSATP but did not affect relaxation to ATP, UTP, adenosine and acetylcholine and ADP. 7. Reactive blue 2 (30 microM) blocked vasodilator responses to ATP, UTP, 2MeSATP and acetylcholine; it was without effect when used at 3 microM. 8. The results of this study show that ATP elicits vasoconstriction of mesenteric arteries of the golden hamster via P2X-purinoceptors located on the smooth muscle, and vasodilatation via P2U-receptors which are located on the endothelium. 2MeSATP has marginal vasodilator activity, suggesting that P2Y-purinoceptors contribute minimally to relaxation to ATP in hamster mesenteric arteries.
摘要
  1. 采用药理学方法对金黄地鼠持续灌注的离体肠系膜动脉血管床中的P2嘌呤受体进行了特性研究。检测了核苷酸ATP、ADP、2-甲硫基ATP(2MeSATP)、α,β-亚甲基ATP(α,β-meATP)和尿苷5'-三磷酸(UTP)引起的血管收缩和舒张反应,以及ATP在交感神经收缩中的作用。2. 在基础张力下,核苷酸引起剂量依赖性血管收缩,观察到的效价顺序为α,β-meATP >> 2MeSATP > ATP = ADP > UTP(基于引起25 mmHg收缩反应所需的剂量)。腺苷在高达5 μmol的剂量下无血管收缩作用。应用单剂量(0.5 μmol)的α,β-meATP后,后续应用核苷酸会使制剂对收缩反应脱敏。3. 电场刺激(4 - 64 Hz,90 V,1 ms,30 s)引起频率依赖性收缩,可被胍乙啶(5 μM)和哌唑嗪(1 μM)消除。4. 非选择性P2嘌呤受体拮抗剂苏拉明(100 μM)对ATP引起的血管收缩反应无显著影响。P2X选择性嘌呤受体拮抗剂磷酸吡哆醛-6-偶氮苯基-2',4'-二磺酸(PPADS,3 μM)几乎完全消除了对ATP的反应。去除内皮后,对ATP和去甲肾上腺素的血管收缩反应增强。5. 在甲氧明(10 - 80 μM)升高张力的制剂中,核苷酸引起血管舒张,观察到的效价顺序为ATP = UTP > ADP >> 腺苷。2MeSATP的血管舒张作用相对较小,在最高测试剂量(50 nmol)时仅引起血管收缩。α,β-meATP不引起血管舒张,但使升高张力的制剂进一步收缩。在ATP和ADP的最高剂量(0.5 μM)时,反应呈双相性,血管收缩先于血管舒张。去除内皮后,除腺苷外,对嘌呤和UTP的血管舒张反应均被消除;在最高剂量时,对ATP、ADP、UTP和2MeSATP的血管收缩明显。6. 苏拉明(100 μM)抑制对ATP和UTP的血管舒张,并消除对2MeSATP的反应。PPADS(3 μM)抑制对2MeSATP的舒张,但不影响对ATP、UTP、腺苷、乙酰胆碱和ADP的舒张。7. 活性蓝2(30 μM)阻断对ATP、UTP、2MeSATP和乙酰胆碱的血管舒张反应;在3 μM使用时无作用。8. 本研究结果表明,ATP通过位于平滑肌上的P2X嘌呤受体引起金黄地鼠肠系膜动脉血管收缩,并通过位于内皮上的P2U受体引起血管舒张。2MeSATP具有微弱的血管舒张活性,表明P2Y嘌呤受体对金黄地鼠肠系膜动脉中ATP引起的舒张作用贡献最小。

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