Morris J L
Centre for Neuroscience, School of Medicine, Flinders University of South Australia, Adelaide.
J Auton Nerv Syst. 1993 Jan;42(1):11-21. doi: 10.1016/0165-1838(93)90337-t.
This study set out to identify the neurotransmitters involved in autonomic vasodilatation of the guinea pig uterine artery. Non-noradrenergic, paracervical neurons supplying this artery contain at least four neuropeptides: vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), dynorphin A (1-17) and somatostatin, probably in addition to acetylcholine. Transmural nerve stimulation of arterial segments precontracted with phenylephrine (3 x 10(-7) mol l-1 and treated with guanethidine (10(-6) mol l-1), produced relaxations which varied in form with the frequency of stimulation and the length of the pulse train. The relaxations were monophasic at low frequencies (< 2 Hz), and were biphasic at higher frequencies (> 5 Hz) and with longer pulse trains (> 50 pulses). Neither phase of the relaxations was reduced by hyoscine (10(-6) mol l-1), or by removal of the endothelium. The faster phase of the relaxations was selectively reduced (by 61%) during treatment with L-nitro-arginine methyl ester (L-NAME; up to 3 x 10(-5) mol l-1). This reduction was reversed by an excess of L-arginine, indicating that the fast relaxation was mediated by nitric oxide, possibly acting as a neurotransmitter. The slower phase of the neurogenic relaxation was preferentially reduced (by 43%) by the endopeptidase, trypsin (1-3 micrograms.ml-1). As VIP is the only currently identified peptide present in the paracervical neurons which causes vasodilatation, it is likely that VIP, or a closely-related peptide, is the transmitter responsible for the slow relaxation. Acetylcholine and an opioid peptide also seem to be released from the vasodilator neurons, but their effects were small, and may have been restricted to pre-synaptic sites. The slower neurogenic relaxations were inhibited by exogenous neuropeptide Y (68% reduction in amplitude), and were slightly potentiated by somatostatin (21% increase in amplitude). Therefore, endogenous stores of these peptides may also contribute to the sum effect of stimulating the paracervical vasodilator neurons. In conclusion, many different substances may act as autonomic co-transmitters from these pelvic vasodilator neurons.
本研究旨在确定参与豚鼠子宫动脉自主血管舒张的神经递质。支配该动脉的非去甲肾上腺素能子宫旁神经元至少含有四种神经肽：血管活性肠肽（VIP）、神经肽Y（NPY）、强啡肽A（1 - 17）和生长抑素，可能还含有乙酰胆碱。用去氧肾上腺素（3×10⁻⁷mol/L）预收缩并用胍乙啶（10⁻⁶mol/L）处理的动脉段进行跨壁神经刺激，产生的舒张反应随刺激频率和脉冲串长度的不同而呈现不同形式。低频（<2Hz）时舒张反应为单相，高频（>5Hz）及较长脉冲串（>50个脉冲）时为双相。东莨菪碱（10⁻⁶mol/L）或去除内皮均不降低舒张反应的任何一个相。在用L - 硝基 - 精氨酸甲酯（L - NAME；高达3×10⁻⁵mol/L）处理期间，舒张反应的较快相选择性降低（降低61%）。过量的L - 精氨酸可逆转这种降低，表明快速舒张是由一氧化氮介导的，一氧化氮可能作为一种神经递质发挥作用。神经源性舒张的较慢相被内肽酶胰蛋白酶（1 - 3μg/ml）优先降低（降低43%）。由于VIP是目前在子宫旁神经元中鉴定出的唯一能引起血管舒张的肽，所以VIP或一种密切相关的肽很可能是负责缓慢舒张的递质。乙酰胆碱和一种阿片肽似乎也从血管舒张神经元释放，但它们的作用较小，可能仅限于突触前部位。较慢的神经源性舒张被外源性神经肽Y抑制（幅度降低68%），被生长抑素轻微增强（幅度增加21%）。因此，这些肽的内源性储存也可能对刺激子宫旁血管舒张神经元的总效应有贡献。总之，许多不同的物质可能作为这些盆腔血管舒张神经元的自主神经共同递质发挥作用。
