ACTIONS OF 4‐AMINOPYRIDINE ON VASCULAR SMOOTH MUSCLE TISSUES OF THE GUINEA‐PIG

Abstract

1 Effects of 4-aminopyridine (4-AP) and procaine on the membrane and contractile properties of smooth muscle cells of the guinea-pig pulmonary artery and portal vein were observed. 2 The membrane potential and length constant of smooth muscle cells of the guinea-pig pulmonary artery were −53.2 mV and 1.2 mm, respectively, and those of the portal vein were −52.6 mV and 0.71 mm, respectively. The membrane was electrically quiescent in the pulmonary artery and it was electrically active in the portal vein. 3 Both 4-AP and procaine depolarized the membrane, increased the membrane resistance and suppressed the rectifying properties in both tissues. Both agents evoked a graded response from the muscle membranes of the pulmonary artery by outward current pulse. Procaine had a greater effect than 4-AP on the above membrane properties. 4 4-AP (10⁻⁵ m) produced contraction without depolarization of the membrane. The contraction evoked by 10⁻⁵ m 4-AP was completely suppressed but that evoked by 5 × 10⁻⁴ m 4-AP was only partly suppressed by phentolamine (10⁻⁷ m). However, the contraction evoked by procaine was not suppressed by phentolamine. 5 4-AP enhanced but procaine suppressed the amplitude of 118 mm [K]₀-induced contraction. 6 The results suggest that 4-AP and procaine suppress K-conductance of the muscle membrane, and 4-AP but not procaine increases noradrenaline release from the nerve terminal. Presumably intracellular free Ca concentrations are also modified by these agents. The effects of 4-AP and procaine on the vascular muscle were compared with those on other excitable tissues.