Bauer Viktor, Sotnikova Ruzena
Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, Dúbravská cesta 9, 841 04 Bratislava, Slovak Republic.
Interdiscip Toxicol. 2015 Mar;8(1):44-7. doi: 10.1515/intox-2015-0008.
The aim of the study was to analyze the involvement of the endothelium in the effects of neutrophils (PMNL) on phenylephrine-precontracted isolated rings of the rat thoracic aorta and to compare their effects with those of peroxynitrite (ONOO(-)) and hypochlorous acid (HOCl). Activated PMNL-induced contraction of the precontracted aorta was prevented by the blockade of NO-synthase and by endothelium removal. In the endothelium-free preparations, the effect of PMNL reappeared in the presence of sodium nitroprusside. The effect of ONOO(-) and HOCl significantly differed from that of activated PMNL both in the presence and absence of the endothelium. It is therefore likely that neither ONOO(-) nor HOCl generated by transformation of superoxide anion radical (O2 (•-)) produced by PMNL is involved in their action. Reduction of the relaxant effect of nitric oxide derived from the endothelium by O2 (•-) seems to be the keystone mechanism in generation of PMNL-induced contraction.
本研究的目的是分析内皮细胞在中性粒细胞(PMNL)对苯肾上腺素预收缩的大鼠胸主动脉离体血管环的作用中的参与情况,并将其作用与过氧亚硝酸盐(ONOO(-))和次氯酸(HOCl)的作用进行比较。一氧化氮合酶的阻断和内皮细胞的去除可防止活化的PMNL诱导的预收缩主动脉收缩。在无内皮细胞的制剂中,在存在硝普钠的情况下,PMNL的作用再次出现。无论有无内皮细胞,ONOO(-)和HOCl的作用均与活化的PMNL的作用显著不同。因此,由PMNL产生的超氧阴离子自由基(O2 (•-))转化生成的ONOO(-)和HOCl似乎均不参与其作用。O2 (•-)对内皮细胞衍生的一氧化氮舒张作用的减弱似乎是PMNL诱导收缩产生的关键机制。