Hashitani Hikaru, Yanai Yoshimasa, Shirasawa Nobuyuki, Soji Tsuyoshi, Tomita Akihiro, Kohri Kenjiro, Suzuki Hikaru
Department of Regulatory Cell Physiology & Nephrourology, Nagoya City University Graduate School of Medical Sciences, Nagoya 467-8601, Japan.
J Physiol. 2005 Dec 15;569(Pt 3):723-35. doi: 10.1113/jphysiol.2005.099309. Epub 2005 Oct 20.
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 mum), sarcoplasmic reticulum Ca2+ pump activity (cyclopiazonic acid, 10 microm), Ca2(+)-activated Cl- channels (niflumic acid, 10 mum) or cyclooxygenase-2 (COX-2; NS-398, 1 microm). 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 microm) 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 microm) or prostaglandin F(2alpha) (0.1 microm), 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.
研究了兔海绵体平滑肌(CCSM)中自发调节与神经介导调节之间的相互作用。记录了等长肌肉张力、细胞内Ca2+浓度([Ca2+]i)和膜电位的变化。CCSM出现自发收缩、[Ca2+]i的瞬时升高(Ca2+瞬变)和去极化。通过阻断L型Ca2+通道(尼卡地平,1 μmol)、肌浆网Ca2+泵活性(环匹阿尼酸,10 μmol)、Ca2(+)-激活的Cl-通道(氟灭酸,10 μmol)或环氧合酶-2(COX-2;NS-398,1 μmol)可消除这种自发活动。根据肌肉张力水平,跨壁神经刺激可引发CCSM的α-肾上腺素能收缩或一氧化氮能舒张。NS-398将神经诱发的收缩抑制约70%,但仅使相应的Ca2+瞬变降低40%。用N(ω)-硝基-L-精氨酸(LNA,100 μmol)阻断一氧化氮合酶可使神经诱发的Ca2+瞬变增强约150%,而相应的Ca2+瞬变仅增加20%。在已用去甲肾上腺素(0.3 μmol)或前列腺素F(2α)(0.1 μmol)预收缩的CCSM制剂中,神经刺激抑制约70%的收缩,且仅使[Ca2+]i降低20%。用COX-2抗体进行荧光免疫组织化学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(PGs)不仅有助于自发收缩的产生,还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,CCSM张力的自发调节与神经介导调节之间的相互作用可能是维持肌肉收缩性的基础。此外,PGs和NO似乎都能改变CCSM张力,而[Ca2+]i只有很小的变化。