What you carry at this position in your DNA and what research says about it.
Hypertension Risk: 9/10 evidence, 58 publications.
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Sample genotype (not yours): G/G
Lower Hypertension Risk but Reduced Beta-Blocker Response
A less active receptor variant helps maintain lower baseline blood pressure but reduces the effectiveness of beta-blocker medications.
What this genotype means: Lower baseline systolic and diastolic blood pressure; Reduced therapeutic response to standard beta-blocker medications; Slightly higher baseline triglyceride levels.
Sample genotype (not yours): C/C
Higher Hypertension Risk but Enhanced Beta-Blocker Response
A highly active receptor variant increases baseline blood pressure risk but makes the heart exceptionally responsive to beta-blocker therapies.
What this genotype means: Increased risk of developing high blood pressure; Highly favorable and robust response to beta-blocker medications; Slightly lower baseline triglyceride levels.
Sample genotype (not yours): G/C
Typical Hypertension Risk and Moderate Beta-Blocker Response
An intermediate genetic profile results in typical baseline blood pressure and a standard response to cardiovascular medications.
What this genotype means: Typical baseline blood pressure and heart rate; Standard response to beta-blocker medications; Average risk profile for cardiovascular diseases.
Gene function and biological role
Gene Function: The ADRB1 gene encodes the beta-1 adrenergic receptor, a key protein found predominantly in cardiac tissue and the kidneys [1]. This receptor binds catecholamines like adrenaline and noradrenaline to regulate heart rate, cardiac contractility, and blood pressure [2]. Activation of these receptors stimulates the sympathetic nervous system, driving the heart's fight-or-flight response [1]. Because of its central role in cardiac function, it is the primary target for beta-blocker medications used to treat hypertension and heart failure [3].
Variant Impact: The rs1801253 variant, often called Gly389Arg, causes a missense mutation that alters the intracellular G-protein coupling domain of the beta-1 adrenergic receptor [4]. Substituting glycine with arginine at position 389 significantly increases the receptor's baseline and agonist-stimulated signaling activity [4]. This gain-of-function change leads to heightened sympathetic nervous system sensitivity, impacting resting blood pressure and heart rate [2]. Consequently, this molecular alteration influences both baseline cardiovascular risk and the clinical efficacy of beta-blocker therapies [1].
Key Insight: The same genetic variant that increases baseline blood pressure also makes the heart significantly more responsive to blood pressure-lowering beta-blocker medications.
Location: ADRB1. Chromosome 10 · 10q25.3 · 114.0 Mb
Estimated prevalence by population
Global 9.7%; European 7.2%; African 16.6%; East Asian 5.6%; South Asian 6.9%; Americas 5.0%; Ashkenazi 14.4%; Finnish 6.6%; Middle Eastern 14.7%; Amish 14.8%.
Estimated GG genotype frequency.
Global 41.3%; European 39.2%; African 48.3%; East Asian 36.2%; South Asian 38.7%; Americas 34.7%; Ashkenazi 47.1%; Finnish 38.2%; Middle Eastern 47.3%; Amish 47.3%.
Estimated GC genotype frequency.
Global 49.0%; European 53.6%; African 35.1%; East Asian 58.2%; South Asian 54.5%; Americas 60.3%; Ashkenazi 38.5%; Finnish 55.2%; Middle Eastern 38.0%; Amish 37.9%.
Estimated CC genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Hypertension
Hypertension. Evidence: 9/10. Source: PMID 38965376. Lower Risk.
Systolic Blood Pressure. Evidence: 10/10. Source: PMID 27618447. Lower.
Diastolic Blood Pressure. Evidence: 9/10. Source: PMID 27841878. Lower.
Lipids & Cholesterol
Triglycerides. Evidence: 9/10. Source: PMID 34887591. Higher.
Pharmacogenomics
Cardiovascular Drug Response
Beta-Blocker Response. Evidence: 6/10. Source: PMID 16844790. Reduced Response.
Showing effects for C/C genotype
Hypertension. Evidence: 9/10. Source: PMID 38965376. Increased Risk.
Systolic Blood Pressure. Evidence: 10/10. Source: PMID 27618447. Higher.
Diastolic Blood Pressure. Evidence: 9/10. Source: PMID 27841878. Higher.
Triglycerides. Evidence: 9/10. Source: PMID 34887591. Lower.
Beta-Blocker Response. Evidence: 6/10. Source: PMID 16844790. Enhanced Response.
Showing effects for G/C genotype
Hypertension. Evidence: 9/10. Source: PMID 38965376. Typical Risk.
Systolic Blood Pressure. Evidence: 10/10. Source: PMID 27618447. Typical.
Diastolic Blood Pressure. Evidence: 9/10. Source: PMID 27841878. Typical.
Triglycerides. Evidence: 9/10. Source: PMID 34887591. Typical.
Beta-Blocker Response. Evidence: 6/10. Source: PMID 16844790. Moderate Response.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele results in a beta-1 adrenergic receptor that exhibits lower baseline and stimulated signaling activity [1]. This natural reduction in receptor activity is associated with lower systolic and diastolic blood pressure, translating to a decreased risk of developing hypertension [2]. However, because the receptors are already less active, beta-blocker medications like metoprolol have less of an active target to block, leading to a blunted therapeutic response [3]. While this means standard beta-blockers may be less effective if needed, the baseline cardiovascular system experiences less chronic adrenaline-driven stress [1]. Some studies suggest a reduced response to specific beta-blockers, so alternatives may be considered [3]. Maintaining a healthy lifestyle remains the primary strategy for cardiovascular wellness.
Lower baseline systolic and diastolic blood pressure; Reduced therapeutic response to standard beta-blocker medications; Slightly higher baseline triglyceride levels.
Sample genotype: CC (Homozygous)
Carrying two copies of the C allele encodes a highly active version of the beta-1 adrenergic receptor, leading to stronger responses to adrenaline [1]. This heightened cellular signaling is associated with elevated baseline systolic and diastolic blood pressure, increasing the risk of hypertension [2]. However, this overactive receptor state makes the cardiovascular system highly sensitive to beta-blocker therapies, which effectively quiet the hyperactive signaling [3]. Clinical studies show that individuals with this genotype experience a more pronounced drop in blood pressure and better overall outcomes when treated with beta-blockers compared to other genotypes [3]. Managing stress, limiting caffeine, and maintaining a low-sodium diet can help mitigate the naturally higher sympathetic nervous system activity.
Increased risk of developing high blood pressure; Highly favorable and robust response to beta-blocker medications; Slightly lower baseline triglyceride levels.
Sample genotype: GC (Heterozygous)
Carrying one G allele and one C allele provides a balanced mix of standard and highly active beta-1 adrenergic receptors on cardiac cells [1]. This intermediate state typically results in average baseline blood pressure and heart rate, representing a standard risk profile for cardiovascular conditions [2]. Because this genotype is common, standard clinical guidelines and typical drug dosages are usually highly applicable [3]. Cardiovascular health is heavily influenced by lifestyle factors such as diet, exercise, and stress management.
Typical baseline blood pressure and heart rate; Standard response to beta-blocker medications; Average risk profile for cardiovascular diseases.
Variants with shared genetic architecture
rs1801252 · ADRB1 Gene · Chr 10 · Beta-Blocker Response
rs12509595 · FGF5 Gene · Chr 4 · Blood Pressure Risk
rs17608766 · GOSR2 Gene · Chr 17 · Blood Pressure
Pharmacogenetics and healthcare outcomes in patients with chronic heart failure.
Content updated August 2026.
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