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MUCOSAL BIOLOGY
Department of Medical Cell Biology, Uppsala University, 751 23 Uppsala, Sweden
Submitted 8 October 2002 ; accepted in final form 6 March 2003
The role of different isoforms of nitric oxide synthase (NOS) in the
gastric mucosal hyperemia, induced by 155 mM luminal hydrochloric acid (pH
0.8) without a barrier breaker, was investigated. Rats were anesthetized
with Inactin (120 mg/kg ip), and mice were anesthetized with Forene (2.2% in
40% oxygen gas at 150 ml/min); the gastric mucosa was exteriorized. Gastric
mucosal blood flow was measured with laser-Doppler flowmetry (LDF) in rats
treated with N
-nitro-L-arginine
(L-NNA; unspecific NOS inhibitor),
L-N6-(1-iminoethyl)lysine [L-NIL;
inducible (i) NOS inhibitor], or S-methyl-L-thiocitrulline
[SMTC; neuronal (n) NOS inhibitor], 10 mg/kg, followed by 3 mg ·
kg–1 · h–1 iv,
in iNOS-deficient (–/–) and nNOS(–/–) mice. mRNA was
isolated from the gastric mucosa in iNOS(–/–) and wild-type (wt)
mice, and real-time RT-PCR was performed. The effect of 155 mM acid on gastric
mucosal permeability was determined by measuring the clearance of
51Cr-EDTA from blood to lumen. LDF increased by 48 ± 13%
during 155 mM HCl luminally, an increase that was abolished by
L-NNA, SMTC, or L-NIL. In iNOS wt mice, LDF increased by
33 ± 8% during luminal acid. The blood flow increase was attenuated
substantially in iNOS(–/–) mice. RT-PCR revealed iNOS mRNA
expression in the gastric mucosa in the iNOS wt groups. The blood flow
increase in response to acid was not abolished in nNOS(–/–) mice
(nNOS-sufficient mice, 39 ± 18%; heterozygous mice, 25 ± 19%;
–/– mice, 19 ± 7%). Mucosal permeability was transiently
increased during 155 mM HCl. The results suggest that iNOS is constitutively
expressed in the gastric mucosa and is involved in acid-induced hyperemia,
suggesting a novel role for iNOS in gastric mucosal protection.
L-N6-(1-iminoethyl)lysine; S-methyl-L-thiocitrulline; gastric mucosal blood flow; laser-Doppler flowmetry; neuronal nitric oxide synthase; in vivo
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