[Potentiation of caffeine-induced contracture by raising extracellular potassium in frog skeletal muscle].
The effect of raising extracellular potassium ([K+]o) on caffeine contracture was investigated, using small bundles dissected from frog anterior tibialis muscle. Elevating [K+]o from the control of 2 mmol/L to 10 or 25 mmol/L significantly potentiated the contracture induced by 3 mmol/L caffeine. The potentiation represented by PKC/PC, where PKC and PC are the peak tension of the caffeine contracture evoked in high and normal [K+]o respectively, was dependent on [K+]o and the duration of conditioning high K+ exposure. With 10 mmol/L [K+]o, the potentiation was gradually increased by prolonging conditioning exposure up to 10 min. On the contrary, with 25 mmol/L [K+]o the potentiation reached a maximum within only 1 min, and then subsided to the control. These different time courses of PKC/PC could not be accounted for by high K+ induced depolarization, but were in general consistence with the time courses of the change in myoplasmic free calcium induced by corresponding high [K+]o. It is suggested that, at least in frog skeletal muscle, the high [K+]o induced potentiation of caffeine contracture is mainly due to an increase of myoplasmic free calcium.
Chen
K Y
KY
Unit of Cell Signal Transduction, Shanghai Institute of Physiology, Chinese Academy of Sciences, Shanghai 200031.
Zhu
P H
PH
D000818:Animals; D001693:Biological Transport, Active; D002110:Caffeine / Q000494:pharmacology*; D003286:Contracture / Q000378:metabolism*; D004357:Drug Synergism; D018482:Muscle, Skeletal / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D011898:Ranidae; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism
D019837:Ryanodine Receptor Calcium Release Channel; D002110:Caffeine; D011188:Potassium