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: The bumetanide-resistant part of forskolin-induced anion secretion in rat colon.
    Author: Schultheiss G, Hörger S, Diener M.
    Journal: Acta Physiol Scand; 1998 Oct; 164(2):219-28. PubMed ID: 9805109.
    Abstract:
    In order to reveal the contribution of the Na(+)-K(+)-2 Cl(-)- cotransporter to forskolin-induced anion secretion, the inhibition of forskolin-stimulated short-circuit current (Isc) by bumetanide, furosemide, azosemide and piretanide was investigated. In the distal colon, all blockers inhibited the forskolin-stimulated Isc with a maximal efficiency of 70%. In contrast, in the proximal colon, bumetanide and furosemide inhibited only about 40% of the forskolin response, whereas piretanide and azosemide were ineffective. A similar result was observed, when Na+ was replaced by impermeant cations suggesting especially in the proximal colon a great part of forskolin-induced anion secretion to be independent of the Na(+)-K(+)-2 Cl(-)-cotransporter. In anion substitution experiments the forskolin-induced increase in Isc was reduced by 70-80%, if either Cl- or HCO3- were omitted from the buffer solution, whereas in the combined absence of both anions the response was nearly suppressed. Measurement of the mucosal alkalinization revealed that forskolin stimulated a HCO3- secretion, which was, however, too weak to explain the bumetanide-insensitive Isc induced by forskolin. Bumetanide inhibited the serosa-to-mucosa flux of Cl- (JsmCl) stimulated by forskolin; an effect, which was strongly enhanced by subsequent administration of the anion exchange inhibitor, SITS. These data suggest that the bumetanide-resistant part of the forskolin-induced Isc is mainly mediated by a basolateral anion exchanger, probably a Cl(-)-HCO3- exchanger, which contributes to forskolin-evoked Cl- secretion, and in addition by a small HCO3- secretion stimulated by the drug.
    [Abstract] [Full Text] [Related] [New Search]