Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder
Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder
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DOI：
10.1152/ajpregu.00656.2010
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发表时间：
2011-08-01
影响因子：
2.8
通讯作者：
Nelson, Mark T.
中科院分区：
文献类型：
--
作者：
Heppner, Thomas J.;Layne, Jeffrey J.;Nelson, Mark T.
赫普纳 TJ、莱恩 JJ、皮尔逊 JM、萨尔基西安 H、纳尔逊 MT。豚鼠膀胱粘膜肌层平滑肌的独特特性。 Am J Physiol Regul Integr Comp Physiol 301：R351-R362，2011。首次发表于 2011 年 6 月 1 日； doi:10.1152/ajpregu.00656.2010.-粘膜肌层是一种位于尿路上皮和膀胱逼尿肌之间的平滑肌，已被描述，尽管其特性和在膀胱功能中的作用尚未得到表征。在这里，使用从豚鼠膀胱中分离出的粘膜组织条，我们发现了似乎起源于粘膜肌层的自发相性收缩（SPC）。该平滑肌层表现出 Ca2+ 波和闪光，但未检测到局部 Ca2+ 事件（Ca2+ 火花、嘌呤能受体介导的瞬变）。 Ca2+ 闪光通常呈爆发式，其发生频率（类似于 5.7 次/分钟）与 SPC（类似于 4 次/分钟）相似，表明 SPC 是由 Ca2+ 闪光爆发触发的。单个粘膜SPC产生的力代表了条带的最大力，而单个逼尿肌SPC产生的力类似于逼尿肌条带最大力的3%。电场刺激（0.5-50 Hz）在孤立的逼尿肌和粘膜条中引起力瞬变。抑制胆碱能受体显着降低逼尿肌和粘膜条的力量（频率较高）。同时抑制嘌呤能和胆碱能受体几乎消除了逼尿肌和粘膜的诱发反应。用 apamin 阻断小电导 Ca2+ 激活的 K+ (SK) 通道不影响粘膜 SPC，而用伊贝里奥毒素 (IbTX) 阻断大电导 Ca2+ 激活的 K+ (BK) 通道则没有变化，表明 SK 和 BK 通道在调节粘膜肌层 SPC 中的作用比在调节逼尿肌 SPC 中的作用小得多。与此一致的是，粘膜肌层肌细胞中的 BK 通道电流密度与逼尿肌细胞中的 20% 相似。这些发现表明，豚鼠的粘膜肌层代表了第二个平滑肌室，其在生理学和药理学上与逼尿肌不同，并且可能有助于膀胱的整体收缩特性。
Heppner TJ, Layne JJ, Pearson JM, Sarkissian H, Nelson MT. Unique properties of muscularis mucosae smooth muscle in guinea pig urinary bladder. Am J Physiol Regul Integr Comp Physiol 301: R351-R362, 2011. First published June 1, 2011; doi:10.1152/ajpregu.00656.2010.-The muscularis mucosae, a type of smooth muscle located between the urothelium and the urinary bladder detrusor, has been described, although its properties and role in bladder function have not been characterized. Here, using mucosal tissue strips isolated from guinea pig urinary bladders, we identified spontaneous phasic contractions (SPCs) that appear to originate in the muscularis mucosae. This smooth muscle layer exhibited Ca2+ waves and flashes, but localized Ca2+ events (Ca2+ sparks, purinergic receptor-mediated transients) were not detected. Ca2+ flashes, often in bursts, occurred with a frequency (similar to 5.7/min) similar to that of SPCs (similar to 4/min), suggesting that SPCs are triggered by bursts of Ca2+ flashes. The force generated by a single mucosal SPC represented the maximal force of the strip, whereas a single detrusor SPC was similar to 3% of maximal force of the detrusor strip. Electrical field stimulation (0.5-50 Hz) evoked force transients in isolated detrusor and mucosal strips. Inhibition of cholinergic receptors significantly decreased force in detrusor and mucosal strips (at higher frequencies). Concurrent inhibition of purinergic and cholinergic receptors nearly abolished evoked responses in detrusor and mucosae. Mucosal SPCs were unaffected by blocking small-conductance Ca2+-activated K+ (SK) channels with apamin and were unchanged by blocking large-conductance Ca2+-activated K+ (BK) channels with iberiotoxin (IbTX), indicating that SK and BK channels play a much smaller role in regulating muscularis mucosae SPCs than they do in regulating detrusor SPCs. Consistent with this, BK channel current density in myocytes from muscularis mucosae was similar to 20% of that in detrusor myocytes. These findings indicate that the muscularis mucosae in guinea pig represents a second smooth muscle compartment that is physiologically and pharmacologically distinct from the detrusor and may contribute to the overall contractile properties of the urinary bladder.