Wang G L, Zhang S S, Li Z H, Liu S F
Department of Pharmacology, Inner Mongolia Medical College, Huhehaote, China.
Zhongguo Yao Li Xue Bao. 1994 May;15(3):279-81.
Effective mechanisms of matrine (Mat) in contraction were observed in isolated rat vasa deferens. Mat caused a strong concentration-dependent contraction of vasa deferens, and this contraction was competitively inhibited by prazosin (Pra, 10 mumol.L-1) and nifedipine (Nif, 50 nmol.L-1), with depression of maximal responses. Their pA2 value was 5.1 and 9.29, respectively. The contraction was also inhibited by verapamil (Ver, 1 mumol.L-1) with depression of maximal responses; but this antagonism was noncompetitive. Its pD2 value was 6.07. Mat promoted CaCl2-induced contraction of vas deferens. The effect of Mat was enhanced in proportion to increase in concentrations of CaCl2. Mat markedly strengthened KCl-induced contraction of vas deferens. The results suggest that one of the mechanisms of the contractive effects of Mat within a certain range of concentrations was related to the activation of the calcium channel.
在离体大鼠输精管中观察了苦参碱（Mat）的收缩作用机制。Mat引起输精管强烈的浓度依赖性收缩，这种收缩被哌唑嗪（Pra，10 μmol·L⁻¹）和硝苯地平（Nif，50 nmol·L⁻¹）竞争性抑制，最大反应降低。它们的pA2值分别为5.1和9.29。维拉帕米（Ver，1 μmol·L⁻¹）也抑制收缩，最大反应降低；但这种拮抗作用是非竞争性的。其pD2值为6.07。Mat促进氯化钙诱导的输精管收缩。Mat的作用随氯化钙浓度增加而增强。Mat显著增强氯化钾诱导的输精管收缩。结果表明，在一定浓度范围内，Mat收缩作用的机制之一与钙通道的激活有关。
