Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.
J Physiol. 2013 Mar 15;591(6):1489-506. doi: 10.1113/jphysiol.2012.247684. Epub 2013 Jan 21.
There is evidence that vasoactive intestinal polypeptide (VIP) participates in inhibitory neuromuscular transmission (NMT) in the internal anal sphincter (IAS). However, specific details concerning VIP-ergic NMT are limited, largely because of difficulties in selectively blocking other inhibitory neural pathways. The present study used the selective P2Y1 receptor antagonist MRS2500 (1 μm) and the nitric oxide synthase inhibitor N(G)-nitro-l-arginine (l-NNA; 100 μm) to block purinergic and nitrergic NMT to characterize non-purinergic, non-nitrergic (NNNP) inhibitory NMT and the role of VIP in this response. Nerves were stimulated with electrical field stimulation (0.1-20 Hz, 4-60 s) and the associated changes in contractile and electrical activity measured in non-adrenergic, non-cholinergic conditions in the IAS of wild-type and VIP(-/-) mice. Electrical field stimulation gave rise to frequency-dependent relaxation and hyperpolarization that was blocked by tetrodotoxin. Responses during brief trains of stimuli (4 s) were mediated by purinergic and nitrergic NMT. During longer stimulus trains, an NNNP relaxation and hyperpolarization developed slowly and persisted for several minutes beyond the end of the stimulus train. The NNNP NMT was abolished by VIP6-28 (30 μm), absent in the VIP(-/-) mouse and mimicked by exogenous VIP (1-100 nm). Immunoreactivity for VIP was co-localized with neuronal nitric oxide synthase in varicose intramuscular fibres but was not detected in the VIP(-/-) mouse IAS. In conclusion, this study identified an ultraslow component of inhibitory NMT in the IAS mediated by VIP. In vivo, this pathway may be activated with larger rectal distensions, leading to a more prolonged period of anal relaxation.
有证据表明,血管活性肠肽(VIP)参与了肛门内括约肌(IAS)的抑制性神经肌肉传递(NMT)。然而,关于 VIP 能 NMT 的具体细节有限,主要是因为难以选择性阻断其他抑制性神经通路。本研究使用选择性 P2Y1 受体拮抗剂 MRS2500(1μm)和一氧化氮合酶抑制剂 N(G)-硝基-L-精氨酸(l-NNA;100μm)阻断嘌呤能和氮能 NMT,以描述非嘌呤能、非氮能(NNNP)抑制性 NMT 以及 VIP 在这种反应中的作用。在非肾上腺素能、非胆碱能条件下,用电刺激(0.1-20Hz,4-60s)刺激神经,并在野生型和 VIP(-/-)小鼠的 IAS 中测量相关的收缩和电活动变化。电刺激引起频率依赖性舒张和超极化,这被河豚毒素阻断。短暂刺激(4s)的反应由嘌呤能和氮能 NMT 介导。在较长的刺激过程中,NNNP 松弛和超极化缓慢发展,并在刺激过程结束后持续数分钟。VIP6-28(30μm)可消除 NNNP NMT,在 VIP(-/-)小鼠中缺失,并被外源性 VIP(1-100nm)模拟。VIP 免疫反应性与肌内神经元一氧化氮合酶的轴突共存,但在 VIP(-/-)小鼠的 IAS 中未检测到。总之,本研究在 IAS 中鉴定了一种由 VIP 介导的抑制性 NMT 的超慢成分。在体内,这种途径可能会被更大的直肠扩张激活,导致更长时间的肛门松弛。