Decreased endothelial nitric oxide synthase in gastric mucosa of
rats with chronic renal failure.
Tomikawa, M., M. Ohta, N. D. Vaziri, J. D. Kaunitz, R. Itani, Z. Ni,
and A. S. Tarnawski.
Department of Medicine, VA Medical Center, Long Beach, California
90822; the University of California, Irvine, California; Department
of Surgery II, Kyushu University, Fukuoka, Japan; VA Medical Center,
Los Angeles, California and the University of California, Los
Angeles, California
APStracts 5:0054F, 1998.
According to recent reports, chronic renal failure (CRF) increases the
susceptibility of gastric mucosa to injury. Since nitric oxide plays
a major role in gastric mucosal defense and injury, we investigated
in rats with CRF produced by 5/6 nephrectomy and in control rats the
expression of nitric oxide synthase in the stomach and measured
mucosal and submucosal gastric blood flow. In CRF rats, gastric
mucosal blood flow was significantly reduced compared with control
rats while submucosal and serosal blood flow was significantly
increased. CRF significantly decreased endothelial nitric oxide
synthase (eNOS) mRNA abundance by 53% (p<0.01) and reduced
expression of eNOS protein by 42% (p<0.01) compared with the
controls. Enzyme activity of eNOS was significantly reduced in
gastric mucosa of CRF rats (p<0.05). These data are consistent with
reduced gastric mucosal blood flow in CRF rats and can explain
altered susceptibility of gastric mucosa to injury in CRF rats.
Received 20 March 1997; accepted in final form 23 February 1998.
APS Manuscript Number F100-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 March 1998