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[硝苯地平对α1肾上腺素能激动剂和去极化溶液引起的大鼠后肢灌注压变化的影响]

[Effect of nifedipine on perfusion pressure changes produced by alpha 1 adrenergic agonists and depolarizing solution in rat hindlimbs].

作者信息

Consolini A, Grand C

机构信息

Area Diseño de Fármacos, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Argentina.

出版信息

Acta Physiol Pharmacol Ther Latinoam. 1991;41(2):229-39.

PMID:1797203
Abstract

The calcium channels blocker, nifedipine (NIF) inhibited in a partial non competitive manner the changes in perfusion pressure (delta P) caused by noradrenaline (NA) in the rat hindquarters, being the maximum inhibition of 31.0 +/- 8.3% (n = 5) for NIF 1.10(-5) M. The vasoconstrictor response of K+ 80 mM - phentolamine 3.10(-6)M was inhibited with lower concentrations of NIF than the one produced by phenylephrine (F) 1.10(-4)M. When the hindquarters were perfused with Krebs OCa-EGTA 2 mM NA developed contractile response. The administration of Ca 2.5 mM after the intracellular calcium store had been depleted, generated vasoconstriction in the presence of F 1.10(-4)M and K+ 80 mM - phentolamine 3.10(-6)M which were blocked in a 60.4 +/- 5.7 (n = 12) and 91.1 +/- 2.3% (n = 10) respectively by NIF 1.10(-5)M. The results suggest that the activation of the adrenergic receptor by NA in the perfused rat hindquarters, probably releases calcium from intracellular stores and promotes calcium influx through pathway scarcely sensitive to NIF. Both mechanisms would be responsible for the partial blockade found in our results.

摘要

钙通道阻滞剂硝苯地平(NIF)以部分非竞争性方式抑制去甲肾上腺素(NA)引起的大鼠后肢灌注压变化(ΔP),NIF 1.10⁻⁵ M时最大抑制率为31.0±8.3%(n = 5)。与1.10⁻⁴ M去氧肾上腺素(F)相比,较低浓度的NIF就能抑制80 mM K⁺ - 3.10⁻⁶ M酚妥拉明引起的血管收缩反应。当后肢用含2 mM EGTA的 Krebs液灌注时,NA产生收缩反应。在细胞内钙库耗竭后给予2.5 mM钙,在1.10⁻⁴ M F和80 mM K⁺ - 3.10⁻⁶ M酚妥拉明存在时产生血管收缩,1.10⁻⁵ M NIF分别以60.4±5.7%(n = 12)和91.1±2.3%(n = 10)的比例阻断这两种情况。结果表明,在灌注的大鼠后肢中,NA激活肾上腺素能受体可能从细胞内储存释放钙,并促进钙通过对NIF几乎不敏感的途径内流。这两种机制可能是我们结果中发现的部分阻断的原因。

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