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P2嘌呤受体对大鼠膀胱平滑肌神经源性收缩的作用

Contribution of P2-purinoceptors to neurogenic contraction of rat urinary bladder smooth muscle.

作者信息

Hashimoto M, Kokubun S

机构信息

Department of Physiology, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Br J Pharmacol. 1995 Jun;115(4):636-40. doi: 10.1111/j.1476-5381.1995.tb14979.x.

Abstract
  1. The contribution of P2-purinoceptors to neurogenic contraction was investigated in rat urinary bladder smooth muscle by measurement of isotonic tension. 2. Contraction of rat urinary bladder smooth muscle induced by electrical stimulation was decreased to 84.19 +/- 3.90% of the control (n = 16) in the presence of atropine (1 microM), which was further decreased to 38.80 +/- 2.75% of the control (n = 49) in the presence of both atropine and 10 microM alpha, beta-methylene adenosine 5'-triphosphate (alpha, beta-Me ATP). 3. The contractile response induced by electrical stimulation in the presence of atropine and alpha, beta-Me ATP was decreased to 27.81 +/- 4.07% (n = 23) and 26.63 +/- 5.01% (n = 15) of the control, by the addition of 100 microM cibacron blue 3GA and 100 microM suramin, respectively. The application of 100 microM adenosine 5'-o-2-thiodiphosphate (ADP beta S) in the presence of atropine and alpha, beta-Me ATP decreased the contractile response induced by electrical stimulations to 17.15 +/- 3.71% (n = 15) of the control. 4. Pretreatment of muscle strips with 100 microM ADP beta S significantly reduced the response to either 200 microM alpha, beta-methylene adenosine 5'-diphosphate or 200 microM ADP beta S. 5. Uridine 5'-triphosphate (100 microM to 1 mM) concentration-dependently contracted muscle strips, and this contraction was significantly antagonized by desensitization of P2-receptors with alpha, beta-Me ATP (10 microM), and completely antagonized by pretreatment of muscle strips with both alpha, beta-Me ATP and ADP beta S (100 microM). 6. Di(adenosine-5') tetraphosphate (30 and 100 microM) contracted muscle strips, whereas it failed to contract after desensitization of P2-receptors.7. It is suggested that about 20% of the neurogenic contraction of rat urinary bladder smooth muscle is mediated via ADP beta S-sensitive purinoceptors.
摘要
  1. 通过测量等张张力,研究了P2嘌呤受体对大鼠膀胱平滑肌神经源性收缩的作用。2. 在存在阿托品(1微摩尔)的情况下,电刺激诱导的大鼠膀胱平滑肌收缩降至对照的84.19±3.90%(n = 16),在同时存在阿托品和10微摩尔α,β-亚甲基腺苷5'-三磷酸(α,β-Me ATP)的情况下,进一步降至对照的38.80±2.75%(n = 49)。3. 在存在阿托品和α,β-Me ATP的情况下,电刺激诱导的收缩反应,分别加入100微摩尔西巴龙蓝3GA和100微摩尔苏拉明后,降至对照的27.81±4.07%(n = 23)和26.63±5.01%(n = 15)。在存在阿托品和α,β-Me ATP的情况下,应用100微摩尔腺苷5'-O-2-硫代二磷酸(ADPβS)将电刺激诱导的收缩反应降至对照的17.15±3.71%(n = 15)。4. 用100微摩尔ADPβS预处理肌条可显著降低对200微摩尔α,β-亚甲基腺苷5'-二磷酸或200微摩尔ADPβS的反应。5. 尿苷5'-三磷酸(100微摩尔至1毫摩尔)浓度依赖性地使肌条收缩,这种收缩被用α,β-Me ATP(10微摩尔)使P2受体脱敏显著拮抗,并用α,β-Me ATP和ADPβS(100微摩尔)预处理肌条完全拮抗。6. 二(腺苷-5')四磷酸(30和100微摩尔)使肌条收缩,而在P

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