High-K medium produces a tonic contraction in guinea pig taenia coli. If muscle strips are preincubated in glucose-free medium, K produces only a phasic contraction. A comparison of Ca45 entry and tissue Ca changes in the two responses were made. Both responses are accompanied by an enhanced uptake of Ca45. In addition to an increased Ca45 uptake, a significant rise of tissue Ca was observed during the tonic contraction. No detectable changes in tissue Ca were noted in the phasic contraction. In light of modern theories of muscle contraction, it was proposed that in the phasic contraction, sufficient Ca is released from a cellular site to initiate contraction, whereas in the tonic contraction enough Ca crosses the membrane to initiate contraction. The transmembrane Ca transport involved in the latter response appeared to be dependent on metabolism.
1 The effects of verapamil and sodium nitroprusside on muscle tension and "4Ca uptake activated in different ways were compared in rabbit aorta, rat aorta and guinea-pig taenia coli.
Further insight into the underlying mechanism(s) of the K-induced phasic and tonic contractions of the taenia coli of the guinea pig was obtained by examining the effects of various metabolic intermediates, inhibitors of metabolism and active transport, on these responses. Evidence is presented to support the thesis that the tonic response is dependent on the aerobic breakdown of carbohydrates and is abolished by substrate removal, a decrease of temperature, DNP, lithium, and ouabain. These same factors have little or no effect on the phasic response. From the evidence presented, it is concluded that the phasic response is a passive process, whereas the tonic contracture is an active one depending on metabolism and possibly linked to active Na transport.
The mode of action of tetrodotoxin on the frog muscle fiber membrane has been analyzed with the aid of intracellular microelectrodes. Tetrodotoxin of 10–7 concentration made the applied cathodal current ineffective in producing action potential, whereas the resting potential and resting membrane resistance underwent little or no change. With 10–8 tetrodotoxin the muscle fibers responded with the small action potentials at high critical depolarizations. These results can be explained on the basis of the membrane being stabilized by inactivation of the sodium-carrying mechanism. Although delayed rectification was not observed in normal muscle fibers, it became apparent in the fibers rendered inexcitable by tetrodotoxin. This finding, together with other evidence in the existing literature, supports an applicability of the sodium theory to the frog muscle fibers.
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