REEVALUATION OF THE SA GENE IN SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS

1. To investigate whether the difference in the SA gene expression in the kidneys is causally related to the pathogenesis of hypertension, w e reassessed the expression of the SA gene in the kidneys of the spont aneously hypertensive rat (SHR), its stroke-prone substrain (SHRSP) an d Wistar-Kyoto (WKY) rat from different sources (SHR/Izm, SHRSP/Izm an d WKY/ Izm from Izumo colony; SHR/Crj and WKY/Crj from Charles River L aboratories). 2. At the age of 5 weeks, high levels of the SA mRNA wer e expressed in the kidneys of SHRSP/Izm, SHR/Izm, SHR/Crj and WKY/Izm, while very low levels of the SA mRNA were observed in those of WKY/Cr j, At the age of 8 weeks, the expression of the SA mRNA in the kidneys of WKY/Izm was at the same level as in those of SHRSP/Izm and two SHR strains. 3. Four genetic markers at the SA locus, an StuI restriction fragment length polymorphism and three microsatellite markers, were n ot polymorphic among Izumo strains of SHR, SHRSP and WKY rats. 4. In s itu hybridization showed strong signals of the SA mRNA in the renal pr oximal tubules, while no positive signals were detected in the glomeru li. 5. Because WKY/Izm has normal blood pressure, our observations ind icate that a simple difference of the SA gene expression in the kidney cannot be an explanation for the difference of blood pressure between SHR(SP)/Izm and WKY/Izm.