These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Glycogenolysis stimulation by non-steroidal anti-inflammatories in the perfused rat liver is not accompanied by Ca2+ release.
    Author: Nascimento EA, Tonon FA, Kelmer-Bracht AM, Bracht A, Ishii-Iwamoto EL.
    Journal: Res Commun Mol Pathol Pharmacol; 1997 May; 96(2):193-201. PubMed ID: 9226753.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]