Endotoxin stimulates fecal pellet output in rats through a neural mechanism

Naunyn Schmiedebergs Arch Pharmacol. 2003 Jan;367(1):51-5. doi: 10.1007/s00210-002-0646-7. Epub 2002 Nov 12.


The effects of endotoxin on fecal pellet output and the neural mechanisms involved in this response were investigated in conscious rats. E. coli endotoxin (40 micro g/kg i.p.) significantly increased fecal excretion for 3 h after the injection. Water content in feces was not modified by endotoxin. Ablation of primary afferent neurons by systemic administration of high doses of capsaicin (20+30+50 mg/kg s.c.) to adult rats prevented the stimulatory effect of endotoxin and so did abdominal vagotomy. Adrenoceptor blockade with phentolamine (5 mg/kg i.p.) + propranolol (3 mg/kg i.p.) did not modify pellet output in endotoxin-treated rats while muscarinic receptor blockade with atropine (1 mg/kg i.p.) abolished the stimulatory effect of endotoxin. Finally, the increase in pellet output induced by endotoxin was prevented in animals receiving the substance P receptor antagonist D-Pro2, D-Trp7,9-substance P (2 mg/kg i.p.) or the NO-synthase inhibitor L-NAME (10 mg/kg i.p.). None of the above treatments modified pellet output in saline-treated rats. These observations indicate that endotoxin increases fecal pellet output through a nervous reflex in which capsaicin-sensitive afferent neurons and the release of excitatory (acetylcholine and substance P) and inhibitory (NO) neurotransmitters in the colonic wall are involved.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Defecation / drug effects*
  • Defecation / physiology
  • Dose-Response Relationship, Drug
  • Endotoxins / pharmacology*
  • Feces*
  • Male
  • Neurons / drug effects*
  • Neurons / physiology
  • Rats
  • Rats, Sprague-Dawley


  • Endotoxins