Abstract
Caffeine (10 or 20 mM)-induced isometric contraction of guinea pig taenia coli showed two successively occurring phasic contractions (I and II) followed by a low sustained tension. Half-time of tension decay in II was 4 ?? 6 times longer than in I. The contraction occasionally showed only a single phasic contraction, of which tension, however, decayed showing two half-times as in two phasic contractions. In the presence of procaine 0.1 ?? 0.5 mM, DNP 0.03 ?? 0.1 mM or Mn2+ 0.5 ?? 1.0 mM, II was entirely abolished whereas I was partially inhibited and such were confirmed by analyzing the time course of tension decay. Maximal tension of I decreased in parallel with lowering the external Na while II was enhanced with 50 ?? 100 mM Na and inhibited by further withdrawal of Na. I and II showed the same Ca-dependecy with respect to the inhibition by Ca deficiency and to the time course of recovery from Ca-free state. Refractoriness tocaffeine after preceding caffeine-contraction also showed little difference between I and II. Sustained tension by caffeine was dependent on Ca in the same manner as tonic K-contracture. Increase in 45Ca uptake with 40 mM K was completely inhibited by 10 mM caffeine while cellular Ca content in the presence of high K markedly increased with caffeine indicating the decrease in Ca exchangeability. The above results indicate that caffeine induced contraction consists of two phasic contractions of which EC-coupling Ca is released from two different cellular sites, and that the phasic contractions are followed by a sustained low tension caused by an increased Ca influx. In the presence of high K, caffeine abolishes the increase in Ca influx by high K and sequesters the sarcoplasmic free Ca resulting in the relaxation of K-contracture.
