When the blood from rabbit or from human was subjected to hemolysis in the test tubes, K-concentration of serum was elevated to about 40 mEq/l. According to these result, the effects of K ion of the concentration up to 30 mM on the contractile response were studied. 2. When the K-concentration was elevated to 10 mM or 20 mM, a transient relaxation was observed. The relaxation, however, was transient and reversed into contraction. No relaxation was observed when K-concentration was elevated gradually. 3. Basilar artery showed higher sensitivity than carotid artery to the elevation of extracellular K-concentration and showed a contractile response to lower K-concentration. Sensitivity to noradrenaline, on the other hand, was lower than that of carotid artery. 4. The contraction by K was stronger in the preparation which showed spontaneous contractions. The contractile response to K was abolished by Ca removal, verapamil (10(-5) M), La (10(-4) M) or Mn (2 mM). 5. Phentramine (2 x 10(-5) M) depressed the contractile response. TTX (5 x 10(-7) g/ml), atropine(10(-6) M) or methysergide (5 x 10(-5) M) showed no effect on the contraction by K. It was suggested that, although the contractile response to elevated K may be due, in part, to the released cathecholamine, it was caused mainly by the direct action of K, especially by its depolarizing action. Since the action was stronger in the preparation which showed spontaneous contraction, the spike activity, in addition to the depolarization, might have important role for this contraction. The contraction may be brought about by influxed Ca caused by the depolarization and/or action potential (Ca spike). It was also suggested that this effect can be one of the cause of the spasm of cerebral blood vessels.
