Interaction between spontaneous and neurally mediated regulation of smooth muscle tone in the rabbit corpus cavernosum
Interaction between spontaneous and neurally mediated regulation of smooth muscle tone in the rabbit corpus cavernosum
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DOI：
10.1113/jphysiol.2005.099309
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发表时间：
2005-12-15
影响因子：
5.5
通讯作者：
Suzuki, H
中科院分区：
文献类型：
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作者：
Hashitani, H;Yanai, Y;Suzuki, H
研究了家兔阴茎海绵体平滑肌（CCSM）自发性和神经介导的张力调节之间的相互作用。记录等长肌张力、细胞内钙浓度（[Ca 2 +]（i））和膜电位的变化。CCSM出现自发性收缩、[Ca 2 +]（i）（Ca 2+瞬变）和去极化一过性增加。通过阻断L型Ca 2+通道（尼卡地平，1 μ M）、肌浆网Ca 2+泵活性（环匹阿尼酸，10 μ M）、Ca 2+激活的Cl-通道（尼氟灭酸，10 μ M）或环氧合酶-2（考克斯-2; NS-398，1 μ M），可消除这种自发活动。刺激脊神经可引起CCSM的α-肾上腺素能收缩或氮能舒张，这取决于肌张力水平。NS-398抑制神经诱发的收缩约70%，但仅导致相应的Ca 2+瞬变减少40%。阻断一氧化氮合酶与N-ω-硝基-L-精氨酸（LNA，100 μ M）加强神经诱发的钙瞬变约150%，而相应的钙瞬变增加只有20%。在用去甲肾上腺素（0.3 μ M）或前列腺素F-2 α（0.1 μ M）预收缩的CCSM制剂中，神经刺激抑制约70%的收缩，仅引起[Ca 2 +]（i）降低20%。考克斯-2抗体荧光免疫组化和逆转录-聚合酶链反应（RT-PCR）方法显示该酶及其mRNA在CCSM中高表达。这些结果表明，自发产生的前列腺素（PG）不仅有助于产生自发收缩，但也促进神经诱发的收缩。相反，自发释放的一氧化氮（NO）抑制兴奋。因此，自发和神经介导的CCSM张力调节之间的相互作用可能是维持肌肉收缩性的基础。此外，PG和NO似乎都改变了CCSM的张力，[Ca 2 +]（i）只有很小的变化。
Interaction between spontaneous and neurally mediated regulation of tone in the corpus cavernosum smooth muscle (CCSM) of the rabbit was investigated. Changes in isometric muscle tension, intracellular Ca2+ concentration ([Ca2+](i)) and membrane potential were recorded. CCSM developed spontaneous contractions, transient increases in [Ca2+](i) (Ca2+ transients) and depolarizations. This spontaneous activity was abolished by blocking L-type Ca2+ channels (nicardipine, 1 mu M), sarcoplasmic reticulum Ca2+ pump activity (cyclopiazonic acid, 10 mu M), Ca2+-activated Cl- channels (niflumic acid, 10 mu M) or cyclooxygenase-2 (COX-2; NS-398, 1 mu M). Transmural nerve stimulation initiated either alpha-adrenergic contractions or nitrergic relaxations of CCSM depending on the level of muscle tone. NS-398 suppressed nerve-evoked contractions by about 70% but caused only a 40% reduction in the corresponding Ca2+ transient. Blocking nitric oxide synthase with N-omega-nitro-L-arginine (LNA, 100 mu M) reinforced nerve-evoked Ca2+ transients by about 150%, whilst increasing the corresponding Ca2+ transients by only 20%. In CCSM preparations that had been pre-contracted with either noradrenaline (0.3 mu M) or prostaglandin F-2 alpha(0.1 mu M), nerve stimulation inhibited about 70% of the contraction and caused only a 20% decrease in [Ca2+](i). Fluorescent immunohistochemistry with COX-2 antibodies and the reverse transcriptase-polymerase chain reaction (RT-PCR) method showed that the enzyme and its mRNA were highly expressed in the CCSM. These results suggest that spontaneously produced prostaglandins (PGs) not only contribute to the generation of spontaneous contractions but also facilitate nerve-evoked contractions. Conversely, spontaneously released nitric oxide (NO) suppresses excitation. Thus, interaction between spontaneous and neurally mediated regulation of CCSM tone may be fundamental to maintaining the muscle contractility. In addition, both PGs and NO appear to alter CCSM tone with only small changes in [Ca2+](i).