EFFECTS OF K+ CHANNEL BLOCKERS ON VASCULAR TONE IN THE PERFUSED RAT LUNG
EFFECTS OF K+ CHANNEL BLOCKERS ON VASCULAR TONE IN THE PERFUSED RAT LUNG
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DOI：
10.1164/ajrccm/144.4.884
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发表时间：
1991-10-01
期刊：
影响因子：
--
通讯作者：
MCMURTRY, IF
中科院分区：
文献类型：
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作者：
HASUNUMA, K;RODMAN, DM;MCMURTRY, IF
为了进一步了解K+通道活性在调节肺血管张力中的作用，我们比较了众多K+通道的差异性阻断剂氯化四乙铵和4-氨基吡啶以及ATP敏感性K+通道抑制剂格列本脲在经甲孕酮处理的盐溶液灌注的大鼠肺中的升压作用。 四乙基铵（1至20 mM）和4-氨基吡啶（1至10 mM），但不是格列本脲（1至20 μ M）引起含氧量正常的肺血管收缩。 Ca++通道阻滞剂硝苯地平（0.1 μ M）和α肾上腺素受体拮抗剂酚妥拉明（10 μ M）抑制4-氨基吡啶反应约50%，并略有减少较小的四乙铵反应。 4-氨基吡啶和（在较小程度上）四乙铵（但不是格列本脲）也增强了血管紧张素II的峰值血管收缩和气道缺氧。 硝苯地平，而不是酚妥拉明，抑制缺氧性血管收缩，并阻止增强4-氨基吡啶。 这些结果表明，Ca++-和/或电压激活（非ATP敏感）的K+通道可能是重要的，在维持低肺血管张力。
To learn more of the role of K+ channel activity in the regulation of pulmonary vascular tone, we compared the pressor effects of the differential blockers of numerous K+ channels, tetraethylammonium chloride and 4-aminopyridine, and the inhibitor of ATP-sensitive K+ channels glibenclamide in meclofenamate-treated salt solution-perfused rat lungs. Tetraethylammonium (1 to 20 mM) and 4-aminopyridine (1 to 10 mM), but not glibenclamide (1 to 20-mu-M) caused vasoconstriction in the normoxic lung. The Ca++ channel blocker nifedipine (0.1-mu-M) and the alpha adrenoceptor antagonist phentolamine (10-mu-M) inhibited the 4-aminopyridine response by about 50% and reduced slightly the smaller tetraethylammonium response. 4-Aminopyridine and, to a lesser extent, tetraethylammonium, but not glibenclamide, also potentiated peak vasoconstriction to angiotensin II and airway hypoxia. Nifedipine, but not phentolamine, inhibited hypoxic vasoconstriction and prevented the potentiation by 4-aminopyridine. These results suggest that Ca++- and/or voltage-activated (not ATP-sensitive) K+ channels may be important in maintaining low pulmonary vascular tone.