Nicotinamide adenine dinucleotide is released from sympathetic nerve terminals via a botulinum neurotoxin A-mediated mechanism in canine mesenteric artery.
Nicotinamide adenine dinucleotide is released from sympathetic nerve terminals via a botulinum neurotoxin A-mediated mechanism in canine mesenteric artery.
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烟酰胺腺嘌呤二核苷酸通过犬肠系膜动脉中的肉毒杆菌神经毒素 A 介导的机制从交感神经末梢释放。
DOI：
10.1152/ajpheart.01062.2005
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
Mutafova-Yambolieva,VioletaN
中科院分区：
文献类型：
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作者：
Smyth,LisaM;Breen,LeanneT;Mutafova-Yambolieva,VioletaN
采用高效液相色谱技术结合荧光和电化学检测，我们发现β-烟酰胺腺嘌呤二核苷酸（β-NAD）在电场刺激（4-16 Hz，0.3 ms，15 V，120 s）下沿着释放。狗离体肠系膜动脉中的ATP和去甲肾上腺素（NE）。β-NAD的释放随着脉冲数/刺激频率而增加。免疫组织化学分析显示酪氨酸羟化酶样免疫反应性（TH-LI）的密集分布和TH-LI阴性神经突起的稀疏分布，表明这些血管主要受交感神经系统控制，并有其他（例如，感觉）神经元。外源性NE（3 μmol/l），α，β-亚甲基ATP（1 μmol/l），神经肽Y（NPY，0.1 μmol/l）、CGRP（0.1 μmol/l），血管活性肠肽（VIP，0.1 μmol/l）和P物质（SP，0.1 μmol/l）对β-NAD的基础释放无影响，提示β-NAD的溢出不是由交感神经递质NE、ATP和NPY引起的，肉毒毒素A（BoNTA，0.1 μmol/l）可阻断4 Hz诱发的NE、ATP和β-NAD的释放，提示在低水平神经活动时，这些神经递质的释放是由25 kDa的N-乙基马来酰亚胺敏感因子附着蛋白受体/突触体相关蛋白介导的胞吐作用所致。然而，在16 Hz下，NE、ATP和β-NAD的诱发释放分别被BoNTA减少了90%、60%和80%，这表明在更高水平的神经活动下，β-NAD可能从突触囊泡的不同群体或神经末梢的不同群体（即，交感神经和感觉末梢）。
Using high-performance liquid chromatography techniques with fluorescence and electrochemical detection, we found that β-nicotinamide adenine dinucleotide (β-NAD) is released in response to electrical field stimulation (4–16 Hz, 0.3 ms, 15 V, 120 s) along with ATP and norepinephrine (NE) in the canine isolated mesenteric arteries. The release of β-NAD increases with number of pulses/stimulation frequencies. Immunohistochemistry analysis showed dense distribution of tyrosine hydroxylase-like immunoreactivity (TH-LI) and sparse distribution of TH-LI-negative nerve processes, suggesting that these blood vessels are primarily under sympathetic nervous system control with some contribution of other (e.g., sensory) neurons. Exogenous NE (3 μmol/l), α,β-methylene ATP (1 μmol/l), neuropeptide Y (NPY, 0.1 μmol/l), CGRP (0.1 μmol/l), vasoactive intestinal peptide (VIP, 0.1 μmol/l), and substance P (SP, 0.1 μmol/l) had no effect on the basal release of β-NAD, suggesting that the overflow of β-NAD is evoked by neither the sympathetic neurotransmitters NE, ATP, and NPY, nor the neuropeptides CGRP, VIP, and SP. Botulinum neurotoxin A (BoNTA, 0.1 μmol/l) abolished the evoked release of NE, ATP, and β-NAD at 4 Hz, suggesting that at low levels of neural activity, release of these neurotransmitters results fromN-ethylmaleimide-sensitive factor attachment protein receptor/synaptosomal-associated protein of 25 kDa-mediated exocytosis. At 16 Hz, however, the evoked release of NE, ATP, and β-NAD was reduced by BoNTA by ∼90, 60, and 80%, respectively, suggesting that at higher levels of neural activity, β-NAD is likely to be released from different populations of synaptic vesicles or different populations of nerve terminals (i.e., sympathetic and sensory terminals).