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豚鼠空肠平滑肌细胞中M胆碱能受体阳离子电流与细胞内钙的关系

Relation between muscarinic receptor cationic current and internal calcium in guinea-pig jejunal smooth muscle cells.

作者信息

Pacaud P, Bolton T B

机构信息

Department of Pharmacology & Clinical Pharmacology, St George's Hospital Medical School, London.

出版信息

J Physiol. 1991 Sep;441:477-99. doi: 10.1113/jphysiol.1991.sp018763.

Abstract
  1. The action of carbachol, which activates muscarinic receptors, was studied in single patch-clamped cells where free internal calcium concentration in the cell (Cai2+) was estimated using the emission from the dye Indo-1. Cells were dialysed with potassium-free caesium solution to block any Ca(2+)-activated K(+)-current. 2. Carbachol applied to the cell evoked an initial peak in Cai2+ followed by a smaller sustained rise (plateau) upon which several oscillations in Cai2+ were often superimposed; the changes in inward, cationic current (icarb) followed changes in Cai2+ closely. Calcium entry blocker did not affect these responses. 3. The initial peak in Cai2+ produced by carbachol was due to calcium store release: it was essentially unchanged at +50 mV, and abolished by prior application of caffeine (10 mM) to the cell or by inclusion of heparin (which blocks D-myoinositol 1,4,5-trisphosphate receptors) in the pipette. In contrast, the rise in Cai2+ produced by ATP in rabbit ear artery smooth muscle cells was unaffected by caffeine or heparin as it was due to calcium entry into the cell. 4. The later sustained rise (plateau) in Cai2+ produced by carbachol was due to the entry of calcium into the cell down its electrochemical gradient as it was affected by changing the cell membrane potential or the calcium concentration of the bathing solution. As the sustained rise in Cai2+ produced by caffeine had similar properties, it was suggested that depletion of calcium stores can evoke an increased calcium entry into the cell through some pathway. 5. The cationic current evoked by carbachol was strongly dependent on Cai2+. It was small if any rise in Cai2+ due to calcium store release was prevented by the inclusion of heparin in the pipette solution and increased greatly if calcium entry was provoked through voltage-dependent channels by applying a depolarizing pulse or if calcium was released from stores by caffeine. 6. In the longitudinal muscle of guinea-pig small intestine, activation of muscarinic receptors by carbachol results in the opening of cationic channels; the resulting depolarization increases the frequency of action potential discharge and this determines the degree of contraction. Muscarinic receptor activation opens cationic channels by two mechanisms: release of stored calcium increases Cai2+ and this strongly potentiates a primary mechanism which may involve a G-protein.
摘要
  1. 在使用染料Indo-1的荧光来估计细胞内游离钙浓度(Cai2+)的单膜片钳细胞中,研究了可激活毒蕈碱受体的卡巴胆碱的作用。用无钾铯溶液透析细胞,以阻断任何Ca(2+)激活的K(+)电流。2. 施加于细胞的卡巴胆碱在Cai2+中引起一个初始峰值,随后是较小的持续升高(平台期),在此之上常叠加有Cai2+的几次振荡;内向阳离子电流(icarb)的变化与Cai2+的变化密切相关。钙通道阻滞剂不影响这些反应。3. 卡巴胆碱产生的Cai2+初始峰值是由于钙库释放:在+50 mV时基本不变,并且在细胞预先应用咖啡因(10 mM)或在移液管中加入肝素(其阻断D-肌醇1,4,5-三磷酸受体)后消失。相比之下,兔耳动脉平滑肌细胞中ATP产生的Cai2+升高不受咖啡因或肝素的影响,因为这是由于钙进入细胞所致。4. 卡巴胆碱产生的Cai2+后期持续升高(平台期)是由于钙顺着其电化学梯度进入细胞,因为它受到改变细胞膜电位或浴液钙浓度的影响。由于咖啡因产生的Cai2+持续升高具有相似的特性,提示钙库耗竭可通过某种途径引起细胞钙内流增加。5. 卡巴胆碱诱发的阳离子电流强烈依赖于Cai2+。如果通过在移液管溶液中加入肝素阻止了因钙库释放导致的Cai2+升高,则电流很小;如果通过施加去极化脉冲经电压依赖性通道激发钙内流,或者通过咖啡因从钙库中释放钙,则电流会大大增加。6. 在豚鼠小肠纵行肌中,卡巴胆碱激活毒蕈碱受体导致阳离子通道开放;由此产生的去极化增加动作电位发放频率,这决定了收缩程度。毒蕈碱受体激活通过两种机制开放阳离子通道:储存钙的释放增加Cai2+,这强烈增强了一种可能涉及G蛋白的主要机制。

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