甲状旁腺激素对冠状动脉的影响。
The coronary effects of parathyroid hormone.
作者信息
Fazekas Réka, Soós Pál, Kékesi Violetta, Fazekas Levente, Juhász-Nagy Alexander
机构信息
Department of Cardiovascular Surgery, Semmelweis University Budapest, Budapest, Hungary.
出版信息
Horm Res. 2004;61(5):234-41. doi: 10.1159/000076628. Epub 2004 Feb 6.
OBJECTIVE
The aim of the present study was to characterize the role of the ATP-sensitive potassium channels (K(+)(ATP)) in the coronary dilator action of parathyroid hormone (PTH).
METHODS
Dose-response curves of intracoronary administrated PTH (0.15-1.33 nmol) were obtained in control phases and during continuous intracoronary administration of the K(+)(ATP) channel-selective antagonist glibenclamide (0.1-1.0 micromol/min) in dogs (n = 13).
RESULTS
Increments of integrated coronary conductance (excess coronary conductance) at PTH doses of 0.15 and 1.33 nmol were 1.17 versus 0.03 ml/mm Hg (p < 0.05) and 4.03 versus 0.94 ml/mm Hg (p < 0.05) in the control versus during maximal blockade, respectively.
CONCLUSION
The results indicate that the activation of K(+)(ATP) channels significantly contributes to the PTH-induced coronary vasodilation.
目的
本研究旨在阐明三磷酸腺苷敏感性钾通道（K(+)(ATP)）在甲状旁腺激素（PTH）冠脉扩张作用中的作用。
方法
在犬（n = 13）中，获取冠脉内给予PTH（0.15 - 1.33 nmol）在对照期以及持续冠脉内给予K(+)(ATP)通道选择性拮抗剂格列本脲（0.1 - 1.0 μmol/min）期间的剂量 - 反应曲线。
结果
在对照期与最大阻断期间，PTH剂量为0.15和1.33 nmol时，冠脉综合传导增加量（额外冠脉传导）分别为1.17对0.03 ml/mm Hg（p < 0.05）和4.03对0.94 ml/mm Hg（p < 0.05）。
结论
结果表明，K(+)(ATP)通道的激活显著促成了PTH诱导的冠脉血管舒张。
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