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Electrogenic ion secretion in proximal, mid and distal colon from fed and starved mice.

Abstract
1. Electrogenic ion transport was monitored in vitro as the short-circuit current (Isc in microA/cm2) across proximal, mid and distal colon removed from fed and 48 hr-starved Swiss albino mice (Mus muscaris). 2. Electrogenic secretion was induced either with serosal bethanechol (muscarinic agonist), DMPP (nicotinic agonist) or dibutyryl-cyclic AMP (DbcAMP). Proximal and distal colon from starved mice showed greater electrogenic secretion in response to bethanechol than those the fed controls while DMPP and DbcAMP did not activate the hypersecretion. 3. In the distal colon, starvation induced a large increase in the basal Isc that was unaffected by mucosal amiloride but was inhibited by tetrodotoxin (TTX) and by diphenylamine-2-carboxylic acid (DPC) unlike the fed basal Isc. Bethanechol activated a biphasic response consisting of a transient decrease in the Isc followed by a sustained increase both of which were significantly greater in the starved than the fed tissue and were inhibited by TTX, DPC and atropine but not hexamethonium. 4. Starvation enhances the secretory response to muscarinic activation in proximal and distal colon and induces an increased basal electrogenic (Cl-) secretion in the distal colon stimulated by an augmented neural tone.
AuthorsV Sagmanligil, R J Levin
JournalComparative biochemistry and physiology. C, Comparative pharmacology and toxicology (Comp Biochem Physiol C Comp Pharmacol Toxicol) Vol. 106 Issue 2 Pg. 449-56 (Oct 1993) ISSN: 0742-8413 [Print] England
PMID7904917 (Publication Type: Journal Article)
Chemical References
  • Tetrodotoxin
  • Dimethylphenylpiperazinium Iodide
  • Bucladesine
Topics
  • Animals
  • Bucladesine (pharmacology)
  • Colon (metabolism, physiology)
  • Dimethylphenylpiperazinium Iodide (pharmacology)
  • Dose-Response Relationship, Drug
  • Fasting (metabolism)
  • In Vitro Techniques
  • Ion Transport (drug effects, physiology)
  • Male
  • Mice
  • Tetrodotoxin (pharmacology)

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