Glycogenolysis stimulation by non-steroidal anti-inflammatories in the perfused rat liver is not accompanied by Ca2+...

Several non-steroidal anti-inflammatories increase glycogenolysis and are also able to affect intracellular Ca2+ channels. In the perfused liver, glycogenolysis stimulation is often associated with a transient Ca2+ efflux, which occurs immediately after the introduction of the glycogenolytic agonist. The purpose of this work was to verify if the introduction of non-steroidal anti-inflammatories also stimulates Ca2+ efflux. Rat livers were pre-loaded with 45Ca2+ in a recirculating system. The anti-inflammatory drugs diclofenac and niflumate were infused 10 minutes after restoration of the once-through perfusion. Glycogenolysis and oxygen uptake stimulation caused by these compounds was not accompanied by any increment in 45Ca2+ release. Subsequent infusion of vasopressin greatly stimulated 45Ca2+ efflux, denoting that the intracellular Ca2+ pools had not been depleted. These results corroborate previous results suggesting that Ca2+ is not involved in glycogenolysis stimulation caused by non-steroidal anti-inflammatories.