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

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Gastrointestinal peptides activate Na(+)-H+ exchanger in AR42J cells by increasing its affinity for intracellular H+.
    Author: Bastié MJ, Williams JA.
    Journal: Am J Physiol; 1990 Jun; 258(6 Pt 1):G958-66. PubMed ID: 1694402.
    Abstract:
    Regulation of intracellular pH (pHi) was studied by dual wavelength fluorometry in monolayers of pancreatic AR42J cells loaded with the fluorescent probe 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In cells superfused with N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solution at pH 7.40, basal pHi was determined to be 7.15 +/- 0.13. Na(+)-H+ exchange could be demonstrated in both resting cells and cells subjected to acid loading by use of transient exposure to NH4Cl. Na(+)-H+ exchange was completely blocked by 300 microM amiloride and was dependent on extracellular Na+ (apparent Km = 25 mM). When the concentration of the NH4Cl pulse was varied (0.5-25 mM), the rate of pHi recovery increased as pHi became acidic, reaching a maximum of 0.007 pH units/s at pHi of 6.4. Gastrointestinal hormones, including pentagastrin, cholecystokinin, and bombesin, increased the rate of Na(+)-H+ exchange without affecting cellular buffer capacity (21.5 +/- 1.8 mM/pH unit), thereby leading to an intracellular alkalinization. This was accompanied by a shift in the curve of Na(+)-H+ exchange as a function of pHi to more alkaline values, although the maximum rate of pH recovery was unchanged. Neither protein kinase C nor Ca2+ could be conclusively linked to activation of Na(+)-H+ exchange, raising the possibility of a more direct, receptor-controlled mechanism.
    [Abstract] [Full Text] [Related] [New Search]