Nishimoto T, Yokoyama M, Fukuzaki H
First Department of Internal Medicine, Kobe University School of Medicine, Japan.
Cardiovasc Res. 1990 May;24(5):364-72. doi: 10.1093/cvr/24.5.364.
The aim of the study was to examine the relationship between phosphoinositide turnover and vascular contraction in response to histamine, and the role of endothelium derived relaxing factor (EDRF) in these activities.
Thoracic aortic strips were studied under isometric tension in an organ bath. Phosphoinositide turnover was studied using [32P]Pi labelling. Cumulative concentration-response curves were obtained for histamine, and for histamine plus H1 and H2 antagonists. The effect of endothelial denudation was examined, as was that of removing Ca2+ from buffer medium, and of adding methylene blue, an inhibitor of EDRF. EXPERIMENTAL PREPARATIONS: Thoracic aortic rings were obtained from 81 male Japanese white rabbits, weight 2.0-2.4 kg.
Histamine (0.1 mumol-0.1 mmol.litre-1) caused concentration dependent contractions and increases of [32P]Pi incorporation into phosphatidylinositol (ED50 = 4.6 mumol.litre-1 and 4.0 mumol.litre-1 respectively). Diphenhydramine inhibited contractile response and phosphatidylinositol labelling by histamine. Cimetidine potentiated contractile response but had no effect on phosphatidylinositol labelling. Endothelial denudation potentiated maximum contraction by 15% and augmented phosphatidylinositol labelling at 0.1 mmol.litre-1 histamine by 30%. In intact aortic rings, methylene blue (10 mumol.litre-1), an inhibitor of EDRF, potentiated histamine induced phosphatidylinositol labelling, but had no influence on denuded rings. A-23187 (0.01 mumol.litre-1), which caused release of EDRF from intact endothelium, suppressed histamine induced phosphatidylinositol labelling in intact aortic rings.
The results suggest that stimulation of the release of EDRF in response to histamine causes self suppression of phosphoinositide turnover and contraction.
本研究旨在探讨磷酸肌醇代谢与组胺引起的血管收缩之间的关系，以及内皮源性舒张因子（EDRF）在这些活动中的作用。
在器官浴槽中，对等长张力下的胸主动脉条进行研究。使用[32P]Pi标记研究磷酸肌醇代谢。获得组胺以及组胺加H1和H2拮抗剂的累积浓度-反应曲线。研究了内皮剥脱的影响，以及从缓冲介质中去除Ca2+和添加EDRF抑制剂亚甲蓝的影响。
从81只体重2.0 - 2.4 kg的雄性日本白兔获取胸主动脉环。
组胺（0.1 μmol - 0.1 mmol·L-1）引起浓度依赖性收缩，并使[32P]Pi掺入磷脂酰肌醇增加（ED50分别为4.6 μmol·L-1和4.0 μmol·L-1）。苯海拉明抑制组胺的收缩反应和磷脂酰肌醇标记。西咪替丁增强收缩反应，但对磷脂酰肌醇标记无影响。内皮剥脱使最大收缩增强15%，并使0.1 mmol·L-1组胺时的磷脂酰肌醇标记增加30%。在完整的主动脉环中，EDRF抑制剂亚甲蓝（10 μmol·L-1）增强组胺诱导的磷脂酰肌醇标记，但对剥脱环无影响。A - 23187（0.01 μmol·L-1）可使完整内皮释放EDRF，抑制完整主动脉环中组胺诱导的磷脂酰肌醇标记。
结果表明，组胺刺激引起的EDRF释放导致磷酸肌醇代谢和收缩的自我抑制。
