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Evidence for a common mechanism for spontaneous rhythmic contraction and myogenic contraction induced by quick stretch in detrusor smooth muscle

机译:逼尿肌平滑肌快速舒张引起自发性节律性收缩和肌源性收缩的常见机制的证据

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AbstractDetrusor smooth muscle exhibits myogenic contraction in response to a quick stretch (QS) as well as spontaneous rhythmic contraction (SRC); however, whether the same population of actomyosin crossbridges with a common regulatory mechanism is responsible for these two types of contraction has not been determined. Detrusor strips from New Zealand white rabbit bladders were allowed to develop SRC at a reference muscle length (Lref), or rhythmic contraction (RC) was induced with tetraethylammonium (TEA). Multiple 10-msec stretches of 15% Lref were then imposed at Lref randomly during the rhythm cycle, and the nadir-to-peak (NTP) tension amplitude of the resulting myogenic contraction was measured. The amplitude and period of the rhythm cycle were measured prior to each QS. NTP was larger when a QS was imposed during a portion the cycle when tension was smaller (n = 3 each SRC and TEA-induced RC). These data suggest that when the rhythmic mechanism was mostly inactive and tension was near a minimum, a larger portion of a shared population of crossbridges was available to produce a myogenic response to a QS. Rho kinase, cyclooxygenase-1, and cyclooxygenase-2 inhibitors (H-1152, SC-560, and NS-398) affected SRC amplitude and NTP amplitude following a QS to the same degree (n = 3 each drug), providing additional evidence to support the hypothesis that a common mechanism is responsible for SRC and myogenic contraction due to QS. If a common mechanism exists, then QS is a potential mechanical probe to study SRC regulation and its alteration in overactive bladder.
机译:摘要逼尿肌平滑肌表现出快速收缩(QS)和自发性节律性收缩(SRC)的肌源性收缩;然而,尚未确定具有共同调控机制的相同的放线菌素跨桥种群是否负责这两种类型的收缩。允许来自新西兰白兔膀胱的逼尿肌条在参考肌肉长度(L )上发展SRC,或用四乙铵(TEA)诱导节律性收缩(RC)。然后在节奏周期内,在L ref 处随机施加10%的15%L ref 多次拉伸,并且将其最低点到峰值(NTP)的张力幅度测量导致的肌源性收缩。在每个QS之前测量节奏周期的幅度和周期。在张力较小的周期的一部分中施加QS时,NTP较大(n = 3,每个SRC和TEA诱导的RC)。这些数据表明,当节律机制大部分不活跃并且张力接近最小时,可以使用共享的跨桥群体中的较大部分来产生对QS的肌源性反应。 Rho激酶,环氧合酶1和环氧合酶2抑制剂(H-1152,SC-560和NS-398)在QS后对SRC振幅和NTP振幅的影响程度相同(每种药物n = 3),提供了更多的证据支持以下假设:一种常见的机制负责QS导致的SRC和肌源性收缩。如果存在共同的机制,那么QS可能是研究SRC调节及其在膀胱过度活动症中的改变的潜在机械探针。

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