1. The membrane potential of smooth muscle cells of the canine coronary artery was - 52 mV, and cells were electrically quiescent. The length and time constant of the membrane were 0.83 mm and 410 msec, respectively. 2. TEA (> 10(-3) M) depolarized the membrane, increased the membrane resistance and suppressed the rectifying property of the membrane. In 10(-2) M-TEA, an outward current pulse evoked a small active response in the canine coronary artery and a large response in the porcine coronary artery. 3. In the canine coronary artery, the minimum [K]o required for contraction was 11.8 mM (-48 mV), and the maximum amplitude of the contraction was evoked in 89 mM-[K]o (-13 mV). The maximum depolarization produced by a tenfold increase in [K]o was 49 mV. 4. In the canine coronary artery, isoprenaline and a low concentration of phenylephrine reduced the resting tension, and a high concentration of phenylephrine (> 5 x 10(-5) M) produced a contraction without affecting the membrane properties. 5. Nitroglycerine reduced resting tension, suppressed the amplitude and raised the threshold of contraction evoked by excess [K]o, electrical depolarization or phenylephrine. In the canine coronary artery, the minimum concentration of nitroglycerine required to suppress K-induced contraction (17.7 mM) was 2.8 x 10(-12) M nitroglycerine. However, resting membrane properties were not affected by 2.8 x 10(-5) M nitroglycerine. TEA induced electrical response was only a little depressed by 2.8 x 10(-5) M nitroglycerine in the porcine coronary artery, while the mechanical response was markedly suppressed. 6. In the canine coronary artery, adenosine (> 10(-5) M) relaxed the tissue in the presence of 17.7 M-[K]o without affecting the membrane property. ACh (> 5 x 10(-5) M) had much the same effects as those observed by treatment with adenosine.