Key result
Genetic variation at the SA gene locus defined by PstI polymorphism was not associated with blood pressure or renal characteristics contributing to the development of hypertension.
Why the study?
Does genetic variation at the SA gene locus influence blood pressure, renal haemodynamics, and the renin-angiotensin system in young adults?
Observational
Does genetic variation at the SA gene locus influence blood pressure, renal haemodynamics, and the renin-angiotensin system in young adults?
Answers are grounded in this paper and cite their sources.
Genetic variation at the SA gene locus defined by the PstI polymorphism does not appear to influence renal characteristics or predispose to hypertension in this population.
The SA gene is expressed in the kidneys and is associated with hypertension in man and experimental animal models. Predisposition to hypertension is associated with renal haemodynamic abnormalities and increased renal SA gene expression. 2. We studied the distribution of the SA gene alleles (A1, A2), defined by the PstI polymorphism, in young adults with contrasting predisposition to hypertension to determine whether genetic variation at the SA gene locus is associated with variations in renal haemodynamics, electrolyte metabolism and the renin-angiotensin system. 3. The frequency of the A2 allele was not significantly different between subjects with high personal and parental blood pressures and subjects with low personal and parental blood pressures. We detected no overall relationship between blood pressures and SA genotype, even after taking sodium intake into account. 4. Glomerular filtration rate, renal blood flow, renal vascular resistance, plasma volume, exchangeable sodium and total body water did not differ according to SA genotypes. Moreover, we detected no significant effect of SA genotype on circulating components of the renin-angiotensin system or atrial natriuretic peptide. 5. In our population, genetic variation at the SA gene locus defined by PstI polymorphism does not influence the renal characteristics that contribute to the development of hypertension.
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Harrap et al. (1995) conducted an observational in Predisposition to hypertension. SA gene alleles (A1, A2) defined by PstI polymorphism vs. Other SA genotypes was evaluated on Blood pressure, renal haemodynamics, electrolyte metabolism, and renin-angiotensin system components. Genetic variation at the SA gene locus defined by PstI polymorphism was not associated with blood pressure or renal characteristics contributing to the development of hypertension.
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