Department of Pharmacology, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
Environ Toxicol Pharmacol. 2005 Sep;20(2):297-304. doi: 10.1016/j.etap.2005.02.007. Epub 2005 Mar 31.
Brief exposure to cobalt chloride augmented vascular contractility. We hypothesized that endothelial dysfunction plays a role in the augmentation of aortic contractility, after brief exposure to cobalt chloride. Rat aortic ring preparations were mounted in organ baths, exposed to cobalt chloride (0.3-300μmol/L) for 30min, and then subjected to contractile agents or relaxants 1 and 5h after the end of exposure. Presence of cobalt chloride did not affect the contractile response to phenylephrine. Brief exposure to cobalt chloride, however, even at 5h after the end of exposure, not only augmented contractile responses to KCl or phenylephrine but also attenuated the relaxant response to acetylcholine. The mechanical denudation of endothelium or inhibition of endothelial nitric oxide synthase with 100μmol/L N(ω)-nitro-l-arginine methyl ester abolished the augmentation of contractile responses. Pre-treatment with 150units/mL of superoxide dismutase also abrogated the augmented contractile responses. Brief exposure to cobalt chloride did not affect the contractile response to phorbol dibutyrate in the presence or absence of calcium, or the expression of HSP70. In conclusion, endothelial dysfunction plays an important role in the augmentation of aortic contractility, after brief exposure to cobalt chloride.
短暂接触氯化钴增强血管收缩性。我们假设内皮功能障碍在短暂接触氯化钴后增强主动脉收缩性中起作用。大鼠主动脉环标本在器官浴中安装，暴露于氯化钴（0.3-300μmol/L）30min，然后在暴露结束后 1 和 5 小时接受收缩剂或松弛剂。钴离子的存在不影响对苯肾上腺素的收缩反应。然而，短暂接触氯化钴，即使在暴露结束后 5 小时，不仅增强了对 KCl 或苯肾上腺素的收缩反应，而且减弱了对乙酰胆碱的松弛反应。机械去除内皮或用 100μmol/L N（ω）-硝基-L-精氨酸甲酯抑制内皮型一氧化氮合酶可消除收缩反应的增强。用 150 单位/mL 的超氧化物歧化酶预处理也消除了增强的收缩反应。短暂接触氯化钴在存在或不存在钙的情况下不影响佛波醇二丁酸酯的收缩反应，也不影响 HSP70 的表达。总之，内皮功能障碍在短暂接触氯化钴后增强主动脉收缩性中起重要作用。
