Cholecystokinin secretagogue-induced gastroprotection: Role of nitric oxide and blood flow

Sonlee D. West, Kenneth S. Helmer, Lily K. Chang, Yan Cui, George H. Greeley, David W. Mercer

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition (nG-nitro-L-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal calcium-dependent NOS activity, but not calcium-independent NOS activity, was increased following CCK and CCK secretagogues. The release of endogenous CCK plays a role in the intrinsic gastric mucosal defense system against injury from luminal irritants. The protective mechanism appears to involve increased production of nitric oxide from primarily the constitutive isoforms of NOS and a resultant increase in blood flow.

Original languageEnglish (US)
Pages (from-to)G399-G410
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number3 47-3
StatePublished - Mar 1 2003
Externally publishedYes


  • Gastric injury
  • Nitric oxide synthase inhibitors
  • Rats
  • Stomach

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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