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: Effects of acetylcholine and caerulein on 86Rb+ efflux in the mouse pancreas. Evidence for a sodium-potassium-chloride cotransport system.
    Author: Singh J.
    Journal: Biochim Biophys Acta; 1984 Aug 08; 775(1):77-85. PubMed ID: 6466663.
    Abstract:
    The effects of acetylcholine and the cholecystokinin-like peptide, caerulein on the fractional efflux of 86Rb+ from preloaded isolated segments of mouse pancreas were studied. Both secretagogues evoked a marked transient increase in 86Rb+ efflux. The removal of Ca2+ from the superfusing medium and addition of 10(-4) M EGTA, markedly reduced, but did not abolish the responses to either acetylcholine or caerulein. Furosemide (10(-5)-10(-3) M) or piretanide (10(-4) M) reduced the basal efflux and inhibited the secretagogue-elicited responses. Stimulus-induced 86Rb+ outflow was abolished when the Cl- component of the superfusing solution was replaced by either NO3-, SO42- or I- but not in case of replacement by Br-. When Na+ was replaced with either Li+ or choline+ both acetylcholine and caerulein failed to elicit any detectable increase in 86Rb+ outflow. However, when Tris+ was substituted for Na+, acetylcholine caused a moderate increase in 86Rb+ efflux which was abolished by either furosemide (10(-4) M) or chloride depletion (nitrate substitution). The removal of extracellular K+ or pretreatment with 10(-3) M ouabain had little effect on secretagogue-evoked 86Rb+ efflux. These results indicate the presence of a diuretic-sensitive Na+-K+-Cl- cotransport system in the mouse pancreatic acinar cell membrane.
    [Abstract] [Full Text] [Related] [New Search]