Actions of 4‐aminopyridine on Vascular Smooth Muscle Tissues of the Guinea‐pig

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 x 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.