What you carry at this position in your DNA and what research says about it.
Hypertension Risk: 5/10 evidence, 20 publications.
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Sample genotype (not yours): A/A
Slightly Increased Hypertension Risk
Slightly higher odds of high blood pressure are associated with this genotype, though the effect is small. It is also associated with a more favorable response to certain blood pressure medications like benazepril.
What this genotype means: Slightly higher risk of high blood pressure; Favorable response to benazepril; Favorable response to imidapril.
Sample genotype (not yours): A/G
Typical Hypertension Risk
Standard blood pressure levels and a typical risk of hypertension characterize this genotype. It is also linked to an enhanced response to specific ACE inhibitor medications.
What this genotype means: Typical risk of hypertension; Favorable response to benazepril.
Sample genotype (not yours): G/G
Slightly Lower Hypertension Risk
Slightly lower odds of developing high blood pressure are associated with this genotype, though the effect is small. It is also linked to a better response to the blood pressure medication candesartan.
What this genotype means: Slightly lower risk of high blood pressure; Favorable response to candesartan.
Gene function and biological role
Gene Function: The CYP11B2 gene encodes aldosterone synthase, a key enzyme responsible for the final steps of aldosterone biosynthesis in the adrenal gland [1]. Aldosterone is a hormone that plays a critical role in regulating blood pressure by controlling sodium and water retention in the kidneys [1]. Variations in this gene can alter enzyme activity and aldosterone levels, directly influencing cardiovascular health and fluid balance [1]. Understanding these genetic differences helps clarify individual susceptibility to high blood pressure and variations in response to cardiovascular medications [2]. Research continues to explore how these genetic markers interact with dietary factors like sodium intake to affect overall heart health [1].
Variant Impact: The rs1799998 variant, also known as the -344C/T polymorphism, is located in the promoter region of the CYP11B2 gene [3]. This genetic change alters a transcription factor binding site, which can modify the rate of gene expression and aldosterone production [3]. The variant is widely studied for its association with essential hypertension, arterial stiffness, and aldosterone-to-renin ratios [1]. It also influences how effectively certain blood pressure medications, such as ACE inhibitors and angiotensin receptor blockers, lower blood pressure [2]. These diverse effects make it one of the most prominent pharmacogenomic and cardiovascular markers in the renin-angiotensin-aldosterone system [3].
Key Insight: The rs1799998 variant is located in the promoter region of the CYP11B2 gene and alters the binding of a transcription factor, directly affecting how much aldosterone synthase is produced.
Location: CYP11B2. Chromosome 8 · 8q24.3 · 142.9 Mb
Estimated prevalence by population
Global 38.7%; European 30.0%; African 59.5%; East Asian 48.9%; South Asian 33.6%; Americas 32.4%; Ashkenazi 21.0%; Finnish 26.6%; Middle Eastern 33.4%; Amish 23.0%.
Estimated AA genotype frequency.
Global 45.3%; European 49.5%; African 35.3%; East Asian 42.1%; South Asian 48.7%; Americas 49.1%; Ashkenazi 49.7%; Finnish 50.0%; Middle Eastern 48.8%; Amish 49.9%.
Estimated AG genotype frequency.
Global 16.0%; European 20.5%; African 5.2%; East Asian 9.0%; South Asian 17.7%; Americas 18.6%; Ashkenazi 29.4%; Finnish 23.5%; Middle Eastern 17.8%; Amish 27.1%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Hypertension
Hypertension. Evidence: 5/10. Source: PMID 26200036. Slightly Increased Risk.
Pharmacogenomics
Cardiovascular Drug Response
Benazepril Response. Evidence: 5/10. Source: PMID 16765146. Stronger Response.
Candesartan Response. Evidence: 5/10. Source: PMID 12065207. Typical Response.
Showing effects for A/G genotype
Hypertension. Evidence: 5/10. Source: PMID 26200036. Typical Risk.
Showing effects for G/G genotype
Hypertension. Evidence: 5/10. Source: PMID 26200036. Slightly Lower Risk.
Benazepril Response. Evidence: 5/10. Source: PMID 16765146. Typical Response.
Candesartan Response. Evidence: 5/10. Source: PMID 12065207. Stronger Response.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Baseline levels of aldosterone synthase activity are typical for those with the A/A genotype, which corresponds to T/T on the opposite strand [1]. Pooled population data place T/T homozygotes at modestly higher odds of essential hypertension than C/C homozygotes, although the effect is small and did not hold in every statistical model. Clinical studies show this genotype is associated with a more pronounced blood pressure-lowering response when treated with angiotensin-converting enzyme (ACE) inhibitors such as benazepril and imidapril [2]. Better outcomes have also been observed with combination therapies like hydralazine and isosorbide dinitrate [3]. These drug-response differences highlight the potential for gene-guided cardiovascular care. Standard medical guidelines do not currently mandate genetic testing before prescribing these therapies.
Slightly higher risk of high blood pressure; Favorable response to benazepril; Favorable response to imidapril.
Sample genotype: AG (Heterozygous)
A single copy of the G allele (corresponding to the C allele on the opposite strand) generally maintains a typical cardiovascular risk profile [1]. Heterozygous individuals sit between the two homozygous groups and carry neither the small increase nor the small decrease in hypertension odds seen at the extremes [1]. From a therapeutic perspective, this genotype is associated with a more favorable blood pressure reduction when using ACE inhibitors like benazepril and imidapril [2]. However, response to other classes of antihypertensive drugs, such as candesartan, remains typical [3]. These findings demonstrate how subtle genetic variations influence drug metabolism and efficacy. Personalized medicine approaches continue to investigate these patterns to optimize treatment plans.
Typical risk of hypertension; Favorable response to benazepril.
Sample genotype: GG (Homozygous)
Elevated rates of aldosterone synthase transcription are more common with the G/G genotype, which corresponds to C/C on the opposite strand [1]. Population data nevertheless run the other way from that laboratory picture: pooled across dozens of observational studies, C/C homozygotes carry about seventeen percent lower odds of essential hypertension than T/T homozygotes, a long-noted paradox. The effect is small and did not hold in every statistical model, so this genotype shifts the odds only slightly. Some studies have also linked this genotype to a higher risk of related cardiovascular complications, such as stroke [2]. Interestingly, clinical research indicates that G/G individuals may respond more effectively to the angiotensin receptor blocker candesartan compared to other genotypes [3].
Slightly lower risk of high blood pressure; Favorable response to candesartan.
Variants with shared genetic architecture
rs11556924 · ZC3HC1 Gene · Chr 7 · Heart Disease Risk
rs604723 · ARHGAP42 Gene · Chr 11 · Blood Pressure Risk
rs1275988 · KCNK3 Gene · Chr 2 · Hypertension and Heart Risk
Genetic variants in the renin-angiotensin-aldosterone system and salt sensitivity of blood pressure.
Variants of the CYP11B2 gene predict response to therapy with candesartan.
Genetic polymorphism of CYP11B2 gene and stroke in the Han Chinese population and a meta-analysis.
Content updated August 2026.
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