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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Differential sodium regulation between salt-sensitive and salt-resistant Sabra rats is not due to any mutation in the renal alpha 2B-adrenoceptor gene.
A defect in sodium modulation of density and agonist affinity of renal alpha 2-adrenoceptor exists in normotensive salt-resistant Sabra (SBN) rats when compared to hypertensive salt-sensitive (SBH). A highly conserved aspartic acid residue in the second helix has been implicated in sodium regulation of alpha 2-adrenoceptor-ligand interactions. As the alpha 2B-adrenoceptor subtype is preponderantly present in kidney of SBH and SBN rats, a mutation might distinguish this subtype between SBH and SBN rats. From this study, no difference between SBH and SBN alpha 2B-adrenoceptor gene could be demonstrated in terms of nucleotide sequence. These data suggest that in Sabra rats, the differential sodium regulation in density and agonist affinity between renal SBH and SBN alpha 2-adrenoceptor may have another origin than the alpha 2B-adrenoceptor encoding gene.[1]
