肾上腺素能受体在Ni2+诱导的冠状动脉收缩中的作用。

G Rubányi, K Hajdú, T Pataki, M Bakos
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引用次数: 0

摘要

在离体灌注大鼠心脏和离体犬冠状动脉条带上研究了肾上腺素能受体可能参与镍离子(Ni2+)诱导的冠状动脉收缩。在两种模型上的实验表明:(1)phenoxybenzamine或phentholamine阻断α -肾上腺素能仅能部分抑制Ni2+诱导的冠状动脉血管收缩;(2)propranolol阻断β -肾上腺素能受体完全阻止Ni2+的作用;(3)Ni2+(1微米)对异丙肾上腺素诱导的冠状动脉血管扩张有显著抑制作用。实验结果表明,α -肾上腺素受体在Ni2+的冠状动脉作用机制中起次要作用(如果有的话),但可能通过β -肾上腺素能机制介导。镍可以改变冠状动脉β -肾上腺素受体的反应性,提示这种微量金属可能在冠状动脉肾上腺素能机制中起调节作用。
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The role of adrenergic receptors in Ni2+-induced coronary vasoconstriction.

The possible involvement of adrenergic receptors in nickel ion (Ni2+)-induced coronary vasoconstriction was studied on isolated perfused rat hearts and on isolated canine coronary artery strips. The experiments on both models showed that (i) alfa-adrenergic blockade by phenoxybenzamine or phentholamine caused only partial depression of Ni2+-induced coronary vasoconstriction: (ii) beta-adrenergic receptor blockade by propranolol totally prevented Ni2+-action, and (iii) Ni2+ (1 microM) caused significant inhibition of coronary vasodilatation induced by isoproterenol. The experimental results indicate that alfa-adrenoceptors play minor role (if any) in the coronary action mechanism of Ni2+ but it may be mediated by beta-adrenergic mechanisms. Nickel was found to alter the reactivity of coronary beta-adrenoceptors suggesting a possible modulatory role of this trace metal in coronary adrenergic mechanisms.

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