Key result
Genetic polymorphisms in ADRB1, ADRB2, ACY3, FGD5, SLC4A1, SLC25A31, PRKCB, DPYS, PAH, and PLEKHH2 are associated with clinical and metabolic responses to beta-blocker therapy in hypertension.
Why the study?
While β-blockers lower blood pressure in hypertension and cardiovascular disease, variations in response and side effects are often influenced by genetic differences affecting drug metabolism and action.
Do genetic polymorphisms influence clinical and metabolic outcomes in patients with hypertension treated with beta-blockers?
Do genetic polymorphisms influence clinical and metabolic outcomes in patients with hypertension treated with beta-blockers?
Genetic polymorphisms in genes such as ADRB1, ADRB2, and PRKCB are associated with variations in clinical and metabolic responses to beta-blockers, supporting the potential for pharmacogenomic personalization in hypertension management.
Answers are grounded in this paper and cite their sources.
May support pharmacogenomic personalization in hypertension; leaves open prospective validation before clinical adoption.
Hypertension is a chronic condition that increases the risk of cardiovascular disease and death. β-blockers, including atenolol, metoprolol, bisoprolol, and carvedilol, lower blood pressure by blocking adrenergic receptors. However, variations in response and side effects are often influenced by genetic differences that affect drug metabolism and action. This narrative review analyzes studies published between 2014 and 2024 in PubMed, ScienceDirect, and Google Scholar using keywords related to genetic variation, β-blockers, hypertension, pharmacogenetics, and polymorphisms. Original studies in English, clinical trials on genetic polymorphisms and β-blocker response were included; reviews and incomplete studies were excluded. Clinical outcomes included changes in systolic and diastolic blood pressure, heart rate, hypotension, aortic root z-score, LVOT gradient, NT-proBNP, and premature ventricular contractions, which were associated with polymorphisms in the ADRB1, ADRB2, ACY3, FGD5, SLC4A1, and SLC25A31 genes. Metabolic outcomes, impaired fasting glucose, new-onset diabetes, and melatonin metabolite changes were associated with variants in PRKCB, DPYS, PAH , and PLEKHH2 . Most data came from European and North American populations, with limited representation from Asia, limiting generalizability. These findings support the use of pharmacogenomics to personalize β-blocker therapy and improve hypertension management, despite challenges related to high costs, limited infrastructure, the lack of clinical guidelines, and population heterogeneity.
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Zulqifli et al. (2026) conducted a review in Hypertension and cardiovascular disease. Beta-blockers (atenolol, metoprolol, bisoprolol, carvedilol) and pharmacogenomic polymorphisms was evaluated on Clinical outcomes (blood pressure, heart rate, hypotension, aortic root z-score, LVOT gradient, NT-proBNP, PVCs) and metabolic outcomes (impaired fasting glucose, new-onset diabetes, melatonin metabolites). Genetic polymorphisms in ADRB1, ADRB2, ACY3, FGD5, SLC4A1, SLC25A31, PRKCB, DPYS, PAH, and PLEKHH2 are associated with clinical and metabolic responses to beta-blocker therapy in hypertension.
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