Abstract
Background Several indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension. Objective To examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat. Design and methods The abundance of NOS mRNA was measured by ...
Abstract
Background Several indications exist to suggest that an impaired production of nitric oxide might have a role in the development of salt-sensitive hypertension. Objective To examine whether the gene expression of the nitric oxide synthases (NOS) is altered in the salt-sensitive Dahl rat compared with that in the salt-resistant Dahl rat. Design and methods The abundance of NOS mRNA was measured by RNase protection assay in different organs of salt-resistant and salt-sensitive Dahl rats. In addition, the zonal expression of NOS genes in the kidney under salt load and salt restriction was determined. Results The abundance of endothelial NOS mRNA was similar between the salt-resistant and salt-sensitive Dahl rat strains in all organs. Inducible NOS mRNA was not detectable by RNase protection assay in any organ. Neuronal NOS (nNOS) mRNA expression, however, was about 50% lower in brain and kidney of salt-sensitive Dahl rats than in salt-resistant Dahl rats. Within the kidney, nNOS mRNA levels were significantly decreased in salt-sensitive Dahl rats compared with those in salt-resistant Dahl rats, in cortex, outer and inner medulla (50, 40 and 30%, respectively) under all dietary conditions. A comparison of renal nNOS gene expression in Dahl rats with that in salt-insensitive Sprague-Dawley rats revealed that the abundance of renal nNOS was similar in salt-sensitive Dahl and Sprague-Dawley rats, but was increased in salt-resistant Dahl rats relative to that in Sprague-Dawley rats. Conclusion These data suggest that nNOS gene expression is increased in salt-resistant Dahl rats compared with that in salt-sensitive Dahl rats. This increased nNOS expression of the salt-resistant Dahl strain might play a part in compensating for a defect of renal salt excretion in the Dahl strains. (C) 2001 Lippincott Williams & Wilkins.
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