Evaluation of vascular actions of the nitric oxide-trapping agent, N-methyl-D-glucamine dithiocarbamate-Fe2+, on basal and agonist-stimulated nitric oxide activity.
Evaluation of vascular actions of the nitric oxide-trapping agent, N-methyl-D-glucamine dithiocarbamate-Fe2+, on basal and agonist-stimulated nitric oxide activity.
复制标题
评估一氧化氮捕获剂 N-甲基-D-葡萄糖胺二硫代氨基甲酸酯-Fe2 对基础和激动剂刺激的一氧化氮活性的血管作用。
DOI：
10.1006/bbrc.1996.0277
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发表时间：
1996
影响因子：
3.1
通讯作者：
Lai,CS
中科院分区：
文献类型：
--
作者：
Pieper,GM;Lai,CS
用NO清除剂N-甲基-D-葡糖胺二硫代氨基甲酸酯铁(MGD-Fe)测定大鼠主动脉内皮细胞自发和激动剂刺激的NO活性。电子顺磁共振波谱证实了MGD-Fe对溶液中NO的无组织清除作用。在静息张力下悬吊的主动脉环上加入MGD-Fe不会引起任何直接收缩，但在用苯肾上腺素收缩的主动脉环上加入MGD-Fe可引起张力的快速增加，而吲哚美辛不能改变这一作用。这种张力增加在用l-硝基精氨酸处理的环或在无内皮细胞的环中没有；然而，这两种情况下形成的张力在大小上与MGD-Fe处理后看到的相似，表明基础NO产生完全被清除。乙酰胆碱产生松弛(最大松弛为100±1%)，这种松弛在l-硝基精氨酸存在或去除内皮后被完全消除。在MGD-Fe(3.0/0.6 mM)存在下，对乙酰胆碱的松弛降低到56±8%。较高浓度的MGD-Fe导致对乙酰胆碱的最大松弛进一步降低；然而，残留成分(约.30%)的放松持续。使用另一种非捕捉剂--羧基-PTIO来模拟这种效果。这些数据表明，MGD-Fe清除激动剂刺激的NO，但也揭示了一种NO合成酶依赖的成分，该成分不能与MGD-Fe相互作用。
The NO scavenger,N-methyl-d-glucamine dithiocarbamate–Fe2+(MGD-Fe), was used to characterize spontaneous and agonist-stimulated NO activity arising from rat aortic endothelium. Scavenging of NO in solution by MGD-Fe without tissue was confirmed by electron paramagnetic resonance spectroscopy. The addition of MGD-Fe to aortic ring segments suspendedin vitrounder resting tension did not cause any direct contraction, but when added to rings contracted with phenylephrine elicited a rapid additional increment in tension which was not altered by indomethacin. This increase in tension was absent in rings pretreated withl-nitroarginine or in rings without endothelium; however, the developed tension in both instances was similar in magnitude to that seen after MGD-Fe suggesting complete scavenging of basal NO production. Acetylcholine produced relaxation (maximum relaxation = 100 ± 1%) which was completely eliminated in the presence ofl-nitroarginine or upon removal of the endothelium. Relaxation to acetylcholine was reduced to 56 ± 8% in the presence of MGD-Fe (3.0/0.6 mM ratio). Higher concentrations of MGD-Fe caused further decreases in the maximum relaxation to acetylcholine; however, a residual component (approx. 30%) of relaxation persisted. This effect was mimicked by using another NO trapping agent, carboxy-PTIO. These data suggest that MGD-Fe scavenges agonist-stimulated NO, but also reveals a NO synthase-dependent component which is unavailable to interact with MGD-Fe.