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The SA gene: predisposition to hypertension and renal function in man
S B Harrap1, N J Samani, D Lodwick
1MRC Blood Pressure Unit, Western Infirmary, Glasgow, U.K.
Clinical Science (London, England : 1979)
|June 1, 1995
Summary
Genetic variation in the SA gene, linked to hypertension, does not appear to affect kidney function or blood pressure regulation in young adults. This study found no association between SA gene alleles and key renal or cardiovascular markers.
Area of Science:
- Nephrology
- Genetics
- Cardiovascular Medicine
Background:
- The SA gene is expressed in the kidneys and has been linked to hypertension in humans and animal models.
- Hypertension predisposition is associated with renal hemodynamic abnormalities and increased renal SA gene expression.
Purpose of the Study:
- To investigate the association between SA gene alleles (A1, A2), defined by PstI polymorphism, and variations in renal hemodynamics, electrolyte metabolism, and the renin-angiotensin system in young adults with differing hypertension predispositions.
- To determine if genetic variation at the SA gene locus influences hypertension development through renal characteristics.
Main Methods:
- Studied the distribution of SA gene alleles (A1, A2) using PstI polymorphism in young adults with high and low blood pressure predispositions.
- Assessed renal hemodynamics (glomerular filtration rate, renal blood flow, renal vascular resistance), plasma volume, exchangeable sodium, total body water, and components of the renin-angiotensin system and atrial natriuretic peptide.
- Analyzed the relationship between SA genotype, blood pressure, and sodium intake.
Main Results:
- No significant difference in the frequency of the A2 allele was found between groups with high and low blood pressure predispositions.
- No overall relationship was detected between blood pressure and SA genotype, even after accounting for sodium intake.
- Glomerular filtration rate, renal blood flow, renal vascular resistance, plasma volume, exchangeable sodium, total body water, renin-angiotensin system components, and atrial natriuretic peptide did not differ significantly across SA genotypes.
Conclusions:
- Genetic variation at the SA gene locus, as defined by the PstI polymorphism, does not appear to influence renal characteristics that contribute to hypertension development in this population.
- The SA gene's role in hypertension may not be mediated through the studied renal hemodynamic and electrolyte parameters in young adults.