Several years ago, it was suggested that Ca++ ions might be involved in the stimulation of sugar permeability seen during muscular contraction (Holloszy & Narabara 1967).
More recently, experiments with epididymal fat pads suggested that lipolytic hormones and metabolic poisons, which stimulate 3-0-methylglucose transport (Clausen 1969a), can induce a release of Ca into the cytoplasm (Clausen 1970). In the isolated rat soleus muscle, hyperosmolarity, metabolic poisons and caffeine, which stimulate 3-0-methylglucose transport (Clausen et al. 1970, Kohn & Clausen 1971) were found to augment the resting tension and the rate coefficient of 45Ca-release (Elbrink et al., in preparation). Furthermore, exposure to Na+free buffers or inhibition of the active Na+-K+-transport, which leads to stimulation of sugar transport in isolated fat cells (Ho et al. 1966, Letarte & Renold 1969), was found to increase the uptake of 45Ca in this preparation (Fig. 1).
These observations suggested that