Differential sodium regulation between salt-sensitive and salt-resistant sabra rats is not due to any mutation in the renal α2B-adrenoceptor gene

A defect in sodium modulation of density and agonist affinity of renal α2-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 α2-adrenoceptor-ligand interactions. As the α2B-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 α2B-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 α2-adrenoceptor may have another origin than the α2B-adrenoceptor encoding gene.