Increased endothelial nitric oxide synthase mRNA level in Bartter's and Gitelman's syndrome. Relationship to vascular reactivity.

Abstract

This overexperession presumably accounts for their increased NO production; thus it could be likely that elevated ecNOS and NO levels are a part of pathophysiological process(es) that leads to their characteristic reduced vascular responses. However, the relationship between the alterations in the NO signalling system observed in this study and the mutations in either Na+-K+-2Cl cotransporter or in a K+ channel ROMK or in Cl- channel ClCNKB in Bartter's syndrome and in Na+-Cl- cotranstransporter in Gitelman's syndrome, recently reported as their primary defects remains to be defined.