Regulation of electrolyte transport by nitric oxide in the mouse cecum.

The effect and role of nitric oxide (NO) in the regulation of ion transport in the mouse cecum were investigated. L-arginine, used to increase NO production, increased short-circuit current (Isc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8+/-65.5 microA/cm2. This increase was not changed in Cl-- or HCO3--free buffers, but was significantly decreased in Na+-free buffer. Using immunohistochemistry, the constitutive form of nitric oxide synthase was found not to be different in the inflamed cecum. The inducible form of the enzyme, however, which was absent in the cecum of normal mice, was present in high levels in the cecum of the colitic mouse. These results suggest that NO causes an increase in Na+ absorption. The increased levels of inducible NO synthase in the inflamed cecum suggest a role for NO in the pathophysiology of inflammatory bowel disease.