尼氟酸的抑制作用去甲肾上腺素,5-hydroxytryptamine-induced加压反应分离肠系膜血管床的老鼠。

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Criddle DN·德·莫拉(RS,格林伍德IA,佤邦

尼氟酸的抑制作用去甲肾上腺素,5-hydroxytryptamine-induced加压反应分离肠系膜血管床的老鼠。

Br J杂志。1997年3月,120 (5):813 - 8。

PubMed ID

9138686 (在PubMed

]

文摘

1。尼氟酸的影响,calcium-activated氯电流的抑制剂,比较与钙通道阻滞剂硝苯地平的行动去甲肾上腺素和5 -羟色胺(5 -)全身加压灌注大鼠反应孤立的肠系膜血管床。2。丸注射去甲肾上腺素(1和10 nmol)灌注压力增加剂量依赖性的方式。硝苯地平(1 microM)抑制1 nmol去甲肾上腺素产生的压力增加了31 + / - 5%。尼氟酸(10和30 microM)也抑制了noradrenaline-induced增加30 microM尼氟酸灌注压力和加压到1 nmol去甲肾上腺素的反应减少了34 + / - 6%。3所示。灌注引起的增加5 -(0.3和3 nmol)是减少尼氟酸浓度的方式(10和30 microM)和30 microM尼氟酸抑制反应0.3和3 nmol 5,分别为49 + / - 8%,50 + / - 7%。硝苯地平(1 microM)减少加压反应3 nmol 5 - 44 + / - 9%。4所示。 In the presence of a combination of 30 microM niflumic acid and 1 microM nifedipine the inhibition of the pressor effects of noradrenaline (10 nmol) and 5-HT (3 nmol) was not significantly greater than with niflumic acid (30 microM) alone. Thus the effects of niflumic acid and nifedipine were not additive. 5. In Ca-free conditions the transient contractions induced by 5-HT (3 nmol) were not reduced by 30 microM niflumic acid, suggesting that this agent does not inhibit calcium release from the intracellular store or the binding of 5-HT to its receptor. 6. Niflumic acid 30 microM did not inhibit the pressor responses induced by KCl (20 and 60 mumol) which were markedly reduced by 1 microM nifedipine. In addition, 1 microM levcromakalim decreased pressor responses produced by 20 mumol KCl. These data suggest that niflumic acid does not block directly calcium channels or activate potassium channels. 7. It is concluded that niflumic acid selectively reduces a component of noradrenaline- and 5-HT-induced pressor responses by inhibiting a mechanism which leads to the opening of voltage-gated calcium channels. Our data suggest that the Ca(2+)-activated chloride conductance may play a pivotal role in the activation of voltage-gated calcium channels in agonist-induced constriction of resistance blood vessels.

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药物

尼氟酸