Samani N J, Lodwick D
Department of Cardiology, Glenfield Hospital, Leicester, UK.
J Hum Hypertens. 1995 Jun;9(6):501-3.
The SA gene was initially identified by differential hybridisation because of its higher expression in the kidney of the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat. In subsequent studies, the allele of the SA gene from the SHR and several other genetically hypertensive strains was found to cosegregate with increased blood pressure in F2 progeny derived from crosses with normotensive rats. The increased expression of the SA gene in the kidney of the SHR occurs early, before the rapid rise in blood pressure in this model, is genotype-dependent and localised to the proximal tubule. Although the functions of its protein product remain to be elucidated, these findings raise the exciting possibilities that: (i) SA represents a major component of an important novel system regulating blood pressure, and (ii) it underlies a primary renal mechanism predisposing to hypertension.
SA基因最初是通过差异杂交鉴定出来的，因为与正常血压的Wistar-Kyoto大鼠相比，它在自发性高血压大鼠（SHR）肾脏中的表达更高。在随后的研究中，发现来自SHR和其他几种遗传性高血压品系的SA基因等位基因，与正常血压大鼠杂交产生的F2子代中血压升高共分离。SA基因在SHR肾脏中的表达增加发生在该模型血压快速升高之前，具有基因型依赖性，且定位于近端小管。尽管其蛋白质产物的功能仍有待阐明，但这些发现提出了令人兴奋的可能性：（i）SA代表调节血压的重要新系统的主要成分，（ii）它是导致高血压的主要肾脏机制的基础。
