Le Jossec M, Cloix J F, Pecquery R, Giudicelli Y, Dausse J P
CJF INSERM 94-02, Service de Biochemie de Paris-Ouest, UFR Biomédicale des Saints-Pères, Paris, France.
Am J Hypertens. 1995 Feb;8(2):177-82. doi: 10.1016/0895-7061(94)00177-D.
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.
与高血压盐敏感（SBH）大鼠相比，血压正常的盐抵抗型Sabra（SBN）大鼠的肾脏α2 - 肾上腺素能受体在钠调节密度和激动剂亲和力方面存在缺陷。第二螺旋中一个高度保守的天冬氨酸残基与α2 - 肾上腺素能受体 - 配体相互作用的钠调节有关。由于α2B - 肾上腺素能受体亚型在SBH和SBN大鼠的肾脏中占主导地位，一个突变可能会区分SBH和SBN大鼠之间的这种亚型。从这项研究来看，SBH和SBN的α2B - 肾上腺素能受体基因在核苷酸序列方面没有差异。这些数据表明，在Sabra大鼠中，肾脏SBH和SBN的α2 - 肾上腺素能受体在密度和激动剂亲和力方面的钠调节差异可能有别于α2B - 肾上腺素能受体编码基因的其他来源。
