Pfaffman M A, Chu-Sun D
Arch Int Pharmacodyn Ther. 1978 Jul;234(1):36-48.
The effects of PGE1 and PGF1alpha (1.4-8.4 X 10(-8)M) were studied on contractures induced by 10--60 mM KCl in the isolated rabbit aorta. The greatest PG-induced increases in the K-contractures were observed at the lower concentrations of KCl. Greater tension increases were noted, particularly at the higher K concentrations with the simultaneous addition of KCl and the PGs rather than with their sequential addition in which the PGs were added after KCl. For example, when the PGs were added to tissues contracted with 60 mM KCl, no additional tension increases occurred, while significant increases were observed when the PGs were added simultaneously with 50--60 mM KCl. Isobolic plots of the data indicate that PGE1 at lower concentrations and PGF1alpha at all concentrations interacted with KCl as competitive antagonists. At median doses PGE1 exhibited an additive effect with KCl, while higher doses interacted in a synergistic manner.
研究了前列腺素E1(PGE1)和前列腺素F1α(PGF1α,浓度为1.4 - 8.4×10⁻⁸M)对离体兔主动脉中由10 - 60mM氯化钾诱导的挛缩的影响。在较低浓度的氯化钾条件下,观察到PG诱导的钾挛缩增加最为明显。在较高的钾浓度下,同时添加氯化钾和PGs时比先添加氯化钾后添加PGs时张力增加更显著。例如,当将PGs添加到用60mM氯化钾收缩的组织中时,没有额外的张力增加,而当PGs与50 - 60mM氯化钾同时添加时,则观察到显著增加。数据的等效应线图表明,较低浓度的PGE1和所有浓度的PGF1α与氯化钾相互作用时表现为竞争性拮抗剂。在中等剂量时,PGE1与氯化钾表现出相加作用,而在较高剂量时则以协同方式相互作用。