Honda H, Sakai Y
Arch Int Pharmacodyn Ther. 1987 Feb;285(2):211-25.
Tension of isolated rings of cerebral and femoral arteries was measured isometrically and Ca2+ movement in these arteries was measured by 45Ca flux to study the mode of action of ifenprodil tartrate (IFT). IFT (10(-7)-10(-4) M) induced relaxation in basilar and femoral arteries contracted by K+ (50 mM). During normoxia (O2 aeration) it induced contraction in arteries contracted by prostaglandin (PG)F2 alpha (10(-5) M), but induced relaxation during hypoxia (N2 aeration). In K+-induced contraction the relaxed tension induced by IFT was reversed by addition of Ca2+ in a dose-dependent manner. The IFT induced relaxation of femoral arteries contracted by K+ was attenuated in Ca2+-free solution containing 0.1 mM EGTA, and the effect of IFT on basilar and femoral arteries contracted by PGF2 alpha was reversed. IFT inhibited K+-induced Ca2+ uptake in cerebral and femoral arteries. IFT enhanced PGF2 alpha-induced Ca2+ uptake in cerebral arteries under normoxia, but inhibited it under hypoxia. The results suggest that the action of IFT may be due to alteration of Ca2+ utilization by vascular cells through blockade of potential-sensitive channels, and this action may reflect regional differences between arteries.
采用等长测量法测定大脑和股动脉离体血管环的张力，通过⁴⁵Ca通量测量这些动脉中的Ca²⁺运动，以研究酒石酸艾芬地尔（IFT）的作用方式。IFT（10⁻⁷ - 10⁻⁴ M）可使由K⁺（50 mM）收缩的基底动脉和股动脉舒张。在常氧（O₂通气）条件下，它可使由前列腺素（PG）F₂α（10⁻⁵ M）收缩的动脉收缩，但在低氧（N₂通气）条件下则引起舒张。在K⁺诱导的收缩中，添加Ca²⁺可呈剂量依赖性地逆转IFT诱导的舒张张力。在含有0.1 mM EGTA的无Ca²⁺溶液中，IFT诱导的由K⁺收缩的股动脉舒张减弱，且IFT对由PGF₂α收缩的基底动脉和股动脉的作用被逆转。IFT抑制大脑和股动脉中K⁺诱导的Ca²⁺摄取。在常氧条件下，IFT增强大脑动脉中PGF₂α诱导的Ca²⁺摄取，但在低氧条件下则抑制该摄取。结果表明，IFT的作用可能是由于通过阻断电压敏感性通道改变了血管细胞对Ca²⁺的利用，且这种作用可能反映了动脉之间的区域差异。
