Objective To study whether the S-A gene locus (on rat chromosome 1) and the sodium potassium ATPase alpha(1) gene locus ton rat chromosome 2) contribute to the elevated blood pressure in the Milan hypertensive rat. Design Go-segregation analysis using polymorphisms in the S-A and Na+/K+-ATPase alpha(1) genes in F-2 rats from a cross of Milan hypertensive and Milan normotensive rats. Analysis of S-A and N+/K+-ATPase alpha(1) gene expression in kidneys of 6 and 25 weeks old Milan hypertensive and normotensive rats. Methods Genotyping of F-2 rat DNA by restriction digestion and Southern blotting and comparison of messenger RNA levels by northern blot analysis. Results Renal expression of S-A was considerably higher in normotensive than it was in hypertensive rats aged 6 and 25 weeks, Despite this difference the S-A genotype did not co-segregate with blood pressure, although the Milan hypertensive rat allele did co-segregate with greater body weight (P = 0.0014) for male F-2 rats, Expression of Na+/K+-ATPase alpha(1) was higher in the kidneys of young hypertensive rats than it was in those of normotensive rats and did not decline with age as occurred in the normotensive rats. However, again the Na+/K+-ATPase alpha(1) genotype did not co-segregate with blood pressure. Conclusions Despite differences in the patterns of expression of S-A and Na+/K+-ATPase alpha(1) genes in the kidneys of Milan hypertensive and normotensive rats, we found no evidence of co-segregation of either gene with blood pressure. Our results suggest that either S-A is simply acting as marker for a linked gene in other crosses for which co-segregation with blood pressure has been observed, or at least, the level of its renal expression is not the sole determinant of its effect on blood pressure, The failure of the Na+/K+-ATPase alpha(1) gene to co-segregate with blood pressure suggests that its greater expression in the kidney of the Milan hypertensive rat is either reactive or controlled by other genetic loci. (C) 1998 Rapid Science Ltd.
Genetic analysis of the S-A and Na+/K+-ATPase alpha(1) genes in the Milan hypertensive rat
CASARI , GIORGIO NEVIO;
1998-01-01
Abstract
Objective To study whether the S-A gene locus (on rat chromosome 1) and the sodium potassium ATPase alpha(1) gene locus ton rat chromosome 2) contribute to the elevated blood pressure in the Milan hypertensive rat. Design Go-segregation analysis using polymorphisms in the S-A and Na+/K+-ATPase alpha(1) genes in F-2 rats from a cross of Milan hypertensive and Milan normotensive rats. Analysis of S-A and N+/K+-ATPase alpha(1) gene expression in kidneys of 6 and 25 weeks old Milan hypertensive and normotensive rats. Methods Genotyping of F-2 rat DNA by restriction digestion and Southern blotting and comparison of messenger RNA levels by northern blot analysis. Results Renal expression of S-A was considerably higher in normotensive than it was in hypertensive rats aged 6 and 25 weeks, Despite this difference the S-A genotype did not co-segregate with blood pressure, although the Milan hypertensive rat allele did co-segregate with greater body weight (P = 0.0014) for male F-2 rats, Expression of Na+/K+-ATPase alpha(1) was higher in the kidneys of young hypertensive rats than it was in those of normotensive rats and did not decline with age as occurred in the normotensive rats. However, again the Na+/K+-ATPase alpha(1) genotype did not co-segregate with blood pressure. Conclusions Despite differences in the patterns of expression of S-A and Na+/K+-ATPase alpha(1) genes in the kidneys of Milan hypertensive and normotensive rats, we found no evidence of co-segregation of either gene with blood pressure. Our results suggest that either S-A is simply acting as marker for a linked gene in other crosses for which co-segregation with blood pressure has been observed, or at least, the level of its renal expression is not the sole determinant of its effect on blood pressure, The failure of the Na+/K+-ATPase alpha(1) gene to co-segregate with blood pressure suggests that its greater expression in the kidney of the Milan hypertensive rat is either reactive or controlled by other genetic loci. (C) 1998 Rapid Science Ltd.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
