K+通道阻断药物和一氧化氮合酶抑制对大鼠肺动脉环缺氧反应的影响

M. R. Karamsetty, R. M. Wadsworth, K. A. Kane
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引用次数: 14

摘要

本研究旨在探讨钾(K+)通道阻滞剂和一氧化氮(NO)合成酶抑制剂l -硝基精氨酸(L-NOARG)对体外大鼠肺内动脉环急性缺氧反应的影响。在大鼠苯肾上腺素预收缩肺动脉环中,缺氧(pO2= 7 mmHg)诱导的反应包括快速发展的初始收缩(第1期)、短暂松弛(第2期)和缓慢发展的持续收缩(第3期),持续时间超过30 min。NOS抑制剂L-NOARG (300 μm)可减弱缺氧反应的第1期和第3期,并放大缺氧反应的第2期。电压门控K+通道阻滞剂4-氨基吡啶(4-AP) (10 mM)也消除了缺氧反应的第3期,放大了第2期。钙活化的K+通道(KCa)阻滞剂四乙基铵(TEA) (20 mM)或白肉毒素(50或200 nM)没有改变缺氧反应,atp依赖性K+通道(KATP)阻滞剂格列本脲(10 μM)也没有改变。L-NOARG (300 μM)和4-AP (10 mM)也能消除碳甾醇诱导的内皮依赖性no介导的松弛。一氧化氮释放剂3-morpholino sydnon亚胺(SIN-1)产生的松弛作用减少4-AP (10 mM)和TEA (20 mM)。数据表明,大鼠肺内动脉环在严重缺氧时一氧化氮的产生减少,这是缺氧收缩持续阶段的基础。这些数据还表明,4-AP敏感的K+通道在NO的释放和作用中起重要作用,因此在缺氧反应中起重要作用。
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Effect of K+ channel blocking drugs and nitric oxide synthase inhibition on the response to hypoxia in rat pulmonary artery rings

  • The aims of this study were to investigate the effects of potassium (K+) channel blockers and the nitric oxide (NO) synthase inhibitor, L-nitroarginine (L-NOARG), on the response produced by acute hypoxia in rat intrapulmonary artery rings in vitro.

  • In rat phenylephrine-precontracted pulmonary artery rings, hypoxia (pO2= 7 mmHg) induced a response which consisted of a rapidly developing initial contraction (phase 1), a transient relaxation (phase 2) and a slowly developing sustained contraction (phase 3) over 30 min. The NOS inhibitor, L-NOARG (300 μm), attenuated phase 1 and 3, and amplified phase 2 of the response to hypoxia. The voltage-gated K+ channel blocker 4-aminopyridine (4-AP) (10 mM) also abolished phase 3 and magnified phase 2 of the response to hypoxia.

  • The hypoxic response was not modified by the calcium-activated K+ channel (KCa) blockers, tetraethylammonium (TEA) (20 mM) or charybdotoxin (50 or 200 nM), nor by the ATP-dependent K+ channel (KATP) blocker, glibenclamide (10 μM).

  • L-NOARG (300 μM) and 4-AP (10 mM) also abolished carbachol-induced endothelium-dependent NO-mediated relaxation. Relaxation produced by the NO releasing agent 3-morpholino sydnonimine (SIN-1) was reduced by 4-AP (10 mM) and TEA (20 mM).

  • The data suggest that NO production is reduced during severe hypoxia in rat intrapulmonary artery rings and that this underlies the sustained phase of the hypoxic contraction. The data also suggests that 4-AP- sensitive K+ channels play an important role in the release andor action of NO, and therefore, in the response to hypoxia.

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Issue Information Autonomic and Autacoid Pharmacology: Goodbye and thank you Attenuation of the anti-contractile effect of cooling in the rat aorta by perivascular adipose tissue Retraction: Dopamine receptor immunohistochemistry in the rat choroid plexus. Issue Information
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