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在大鼠离体肺血管床中,UTP、ATP及相关核苷酸通过P2嘌呤受体介导血管收缩的证据。

Evidence for a P2-purinoceptor mediating vasoconstriction by UTP, ATP and related nucleotides in the isolated pulmonary vascular bed of the rat.

作者信息

Rubino A, Burnstock G

机构信息

Department of Anatomy and Developmental Biology, University College London.

出版信息

Br J Pharmacol. 1996 Jul;118(6):1415-20. doi: 10.1111/j.1476-5381.1996.tb15554.x.

Abstract
  1. The vasoconstrictor effects of uridine 5'-triphosphate (UTP), uridine 5'-diphosphate (UDP), uridine 5'-monophosphate (UMP) and uridine were tested in the isolated pulmonary vascular bed of the rat. Comparison was made with the effects of adenine nucleotides, adenosine 5'-triphosphate (ATP), adenosine 5'-diphosphate (ADP), adenosine 5'-monophosphate (AMP) and with adenosine. The effect of P2x-purinoceptor desensitization and blockade was compared on the vascular responses to uracil and adenine nucleotides. 2. At doses ranging from 10(-8) to 10(-5) mol, UTP elicited dose-dependent vasoconstriction. UDP was equiactive to UTP, while UMP and uridine did not show vasomotor activity. Similarly, ATP showed dose-related vasoconstrictor activity. ADP was less potent than ATP in eliciting vasoconstriction, while AMP was active only at the higher doses tested and adenosine was ineffective. 3. Vasoconstriction was produced by ATP analogues with the following order of potency: alpha, beta-methylene ATP > ATP gamma S > beta, gamma-methylene ATP > 2-methylthio ATP > or = ATP. 4. Desensitization of P2x-purinoceptors by the selective agonist alpha, beta-methylene ATP did not modify the vasoconstrictor activity of UTP and UDP and only partially reduced vasoconstrictor responses to ATP, while it abolished vascular responses to alpha, beta-methylene ATP itself. 5. The antagonists of P2-purinoceptors, suramin and pyridoxalphosphate-6-azophenyl-2', 4'-disulphonic acid (PPADS), did not affect vascular responses to UTP and UDP, but reduced vasoconstriction evoked by beta, gamma-methylene ATP and ATP by about 70 and 30%, respectively. 6. This study demonstrates that uracil nucleotides, UTP and UDP, elicit vasoconstriction in the rat pulmonary vascular bed. In addition to confirming the presence of classical P2x-purinoceptors, these results also suggest the presence of a distinct purinoceptor subtype which mediates UTP- and ATP- evoked vasoconstriction in the rat pulmonary circulation.
摘要
  1. 在大鼠离体肺血管床中测试了尿苷5'-三磷酸(UTP)、尿苷5'-二磷酸(UDP)、尿苷5'-单磷酸(UMP)和尿苷的血管收缩作用。将其与腺嘌呤核苷酸、腺苷5'-三磷酸(ATP)、腺苷5'-二磷酸(ADP)、腺苷5'-单磷酸(AMP)以及腺苷的作用进行了比较。比较了P2x嘌呤受体脱敏和阻断对血管对尿嘧啶和腺嘌呤核苷酸反应的影响。2. 在10^(-8)至10^(-5)摩尔的剂量范围内,UTP引起剂量依赖性血管收缩。UDP与UTP活性相当,而UMP和尿苷未表现出血管运动活性。同样,ATP表现出剂量相关的血管收缩活性。ADP在引起血管收缩方面的效力低于ATP,而AMP仅在测试的较高剂量时具有活性,腺苷则无作用。3. ATP类似物产生血管收缩作用的效力顺序如下:α,β-亚甲基ATP > ATPγS > β,γ-亚甲基ATP > 2-甲硫基ATP > 或 = ATP。4. 选择性激动剂α,β-亚甲基ATP对P2x嘌呤受体的脱敏并未改变UTP和UDP的血管收缩活性,仅部分降低了对ATP的血管收缩反应,而它消除了血管对α,β-亚甲基ATP自身的反应。5. P2嘌呤受体拮抗剂苏拉明和吡哆醛磷酸-6-偶氮苯基-2',4'-二磺酸(PPADS)不影响血管对UTP和UDP的反应,但分别使β,γ-亚甲基ATP和ATP引起的血管收缩降低约70%和30%。6. 本研究表明,尿嘧啶核苷酸UTP和UDP在大鼠肺血管床中引起血管收缩。除了证实经典P2x嘌呤受体的存在外,这些结果还提示存在一种独特的嘌呤受体亚型,其介导大鼠肺循环中UTP和ATP引起的血管收缩。

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