Diastolic Blood Pressure Change
Introduction
Section titled “Introduction”Diastolic blood pressure (DBP) change refers to the variation in the lower number of a blood pressure reading, often observed over a 24-hour period. This dynamic aspect of blood pressure, particularly the nocturnal fall or “dipping,” is a crucial physiological indicator. Blood pressure naturally decreases during sleep, and the extent of this reduction, or lack thereof, can have significant health implications. Understanding DBP change involves not only its direct but also the genetic and environmental factors that influence its patterns.
Background
Section titled “Background”Blood pressure exhibits a circadian rhythm, typically dropping during nighttime hours. This phenomenon is known as nocturnal blood pressure dipping. Conversely, a reduced nocturnal fall, termed “non-dipping,” or even a rise in blood pressure during the night (“reverse dipping”), are recognized patterns. Ambulatory blood pressure monitoring (ABPM) is a standard method used to assess these patterns, involving frequent blood pressure measurements throughout the day and night . Even in larger meta-analyses, specific sub-group analyses, like heritability estimates for African Americans, could not be performed due to insufficient sample sizes, which impedes a comprehensive understanding of genetic influences across diverse populations.[1] Furthermore, the consistency of replication for all identified variants across different datasets remains a challenge. Some initial associations in discovery analyses did not show additional evidence in replication datasets, a phenomenon that can be attributed to factors such as varying linkage disequilibrium patterns between populations or differences in variant filtering during quality control procedures.[1] This inconsistent replication can lead to an overestimation of effect sizes for initially significant findings and raises questions about the robustness and universal applicability of some genetic associations, potentially limiting their clinical translation.
Generalizability and Phenotype Definition
Section titled “Generalizability and Phenotype Definition”The generalizability of findings is constrained by the population diversity represented in the studies. Research primarily focused on individuals of European American and African American ancestries, with some inclusion of Latino/Brazilian populations.[1]The inability to estimate heritability in African American individuals due to limited sample size represents a critical gap in understanding the genetic architecture of diastolic blood pressure change within this specific demographic.[1] This restricted ancestral representation limits the direct applicability of findings to other global populations, where distinct genetic backgrounds and environmental influences may play a different role in blood pressure regulation.
Additionally, the definition and of “diastolic blood pressure change” vary considerably across different studies, which impacts the direct comparability and synthesis of results. Some studies define this as a “trajectory,” representing the rate of change per year derived from complex mixed-effects models over multiple visits.[1] while others might use average residuals across available visits or focus on specific patterns like nocturnal dipping.[2] Moreover, the number of longitudinal measurements available per individual can differ, with some cohorts having only a single examination for a majority of participants, which can compromise the accuracy and reliability of estimated longitudinal change.[2] Such heterogeneity in phenotype construction can introduce variability, complicating efforts to build a unified understanding of the underlying genetic factors.
Environmental Confounders and Knowledge Gaps
Section titled “Environmental Confounders and Knowledge Gaps”While studies incorporated adjustments for several key covariates, including age, sex, body mass index (BMI), and the use of antihypertensive medications.[1]the intricate influence of numerous environmental and lifestyle factors on diastolic blood pressure change cannot be fully accounted for. Detailed information on factors such as dietary patterns, levels of physical activity, chronic stress, socioeconomic status, and other unmeasured environmental exposures are known to significantly affect blood pressure trajectories but are often challenging to comprehensively quantify and integrate into genetic models. The omission of these granular environmental data may obscure the true genetic effects and limit the identification of crucial gene-environment interactions.
Despite the identification of new genetic loci, a substantial portion of the heritability for diastolic blood pressure change remains unexplained, particularly for trajectory-based phenotypes.[1]This phenomenon, often referred to as “missing heritability,” suggests that many genetic influences are yet to be discovered, potentially involving rare genetic variants, complex polygenic interactions, or dynamic epigenetic mechanisms that are not fully captured by current genome-wide association study designs. The current analytical models, while robust, may not entirely encompass all biological complexities, including gene-gene interactions or the temporal dynamics of gene expression, thereby leaving significant gaps in the complete understanding of diastolic blood pressure regulation.
Variants
Section titled “Variants”Genetic variations play a crucial role in influencing an individual’s predisposition to various physiological traits, including the regulation of diastolic blood pressure. These variants, often single nucleotide polymorphisms (SNPs), are located within genes or in regions that regulate gene activity, impacting fundamental cellular processes, vascular function, and metabolic pathways. Understanding their associations can provide insights into the complex genetic architecture underlying blood pressure maintenance and response to interventions.
Variants in genes like ULK4, GEMIN2P2, and TP53are associated with core cellular functions that indirectly affect cardiovascular health.ULK4 (Unc-51 Like Autophagy Activating Kinase 4) is involved in autophagy, a critical process for cellular waste removal and recycling, which maintains cellular homeostasis. GEMIN2P2 (Gem (nuclear organelle) Associated Protein 2) plays a role in small nuclear ribonucleoprotein (snRNP) biogenesis, essential for gene expression. Disruptions in these fundamental cellular processes can lead to cellular stress and inflammation, influencing vascular health and blood pressure regulation. The TP53gene, a well-known tumor suppressor, is involved in cell cycle control, DNA repair, and programmed cell death. Its broad influence on cellular integrity and stress responses can impact the health and function of blood vessels, thereby affecting diastolic blood pressure over time.[1], [3] Other variants affect genes involved in transport, signaling, and developmental pathways. The rs13107325 variant in SLC39A8 (Solute Carrier Family 39 Member 8) relates to zinc transport, a vital process for numerous enzymes and transcription factors that regulate immune responses, oxidative stress, and vascular remodeling, all of which influence blood pressure. The intergenic region encompassing PRDM8 (PR/SET Domain 8) and FGF5 (Fibroblast Growth Factor 5), with a variant like rs13125101 , may impact developmental processes and cellular signaling pathways that shape vascular structure and function. CASZ1(Caspase Recruitment Domain Family Member 1), a zinc finger transcription factor, is involved in neurogenesis and development, potentially influencing the nervous system’s regulation of blood pressure. These genetic influences contribute to the intricate mechanisms governing blood pressure, including diastolic blood pressure changes.[4], [5]Variants impacting vascular function and metabolic links also hold significance for diastolic blood pressure. Thers1275923 variant in KCNK3(Potassium Two Pore Domain Channel Subfamily K Member 3) may alter the activity of potassium channels, which are crucial for regulating the electrical excitability of cells, including vascular smooth muscle cells, directly influencing vascular tone. Thers1887320 variant, located in the intergenic region of LINC01752 and LINC02871, points to the role of long non-coding RNAs in regulating gene expression and cellular processes vital for vascular health. JCAD (Junctional Cadherin 5 Associated) is important for maintaining the integrity and function of endothelial cell junctions, which are critical for vascular barrier function. Furthermore, variants in ABO, such as rs115478735 , are linked to broader cardiovascular risk factors and blood pressure regulation, possibly through effects on coagulation and inflammation. Similarly,INSR(Insulin Receptor) variants, includingrs12978472 and rs77431689 , are highly relevant due to the strong association between insulin resistance, impaired insulin signaling, and the development of hypertension, which directly impacts diastolic blood pressure.[6], [7]
Key Variants
Section titled “Key Variants”Definition and of Diastolic Blood Pressure Change
Section titled “Definition and of Diastolic Blood Pressure Change”Diastolic blood pressure (DBP) represents the minimum arterial pressure during ventricular relaxation and is a fundamental physiological indicator of cardiovascular health. The concept of “diastolic blood pressure change” encompasses various dynamic aspects of DBP, notably “nocturnal blood pressure dipping” and “DBP trajectory”.[4] Nocturnal dipping specifically refers to the physiological decrease in DBP during sleep compared to waking hours, often quantified as a “night-to-day BP ratio,” which expresses night-time DBP as a percentage of daytime DBP.[4]Understanding these changes is crucial for assessing cardiovascular risk beyond a single static .
The precise of DBP change relies heavily on standardized methodologies. Ambulatory Blood Pressure (ABPM) is a key approach, employing devices such as the Microlife WatchBP O3 monitor to record blood pressure at regular intervals over a 24-hour period.[4] Typically, measurements are taken every 20 minutes during the day (e.g., 7 am to 10 pm) and every 30 minutes during the night (e.g., 10 pm to 7 am), with specific operational definitions for mean daytime and night-time DBP values.[4]To ensure data quality, single observations are excluded if they meet criteria such as low pulse pressure (<15 mmHg if SBP < 120 mmHg, <20 mmHg if SBP > 120 mmHg), high heart rates (≥110 bpm), or inappropriate physical activity or body position during.[4] A recording is generally considered acceptable if it contains more than 15 daytime and more than 7 night-time measurements.[4] For clinic-based measurements, a common practice involves taking multiple readings after a five-minute rest, discarding the first to mitigate the “white coat syndrome” effect, and averaging the subsequent readings.[7]
Classification and Clinical Thresholds
Section titled “Classification and Clinical Thresholds”The classification of DBP change patterns provides valuable diagnostic and prognostic insights. A key classification system for nocturnal dipping categorizes individuals based on their night-to-day BP ratio. A “non-dipper” is precisely defined as an individual whose night-to-day DBP ratio is greater than 90%.[4]This categorical approach identifies individuals who do not exhibit the expected physiological nocturnal decline in blood pressure, a pattern often associated with increased cardiovascular risk. This contrasts with “dippers,” who show a more pronounced nocturnal fall in DBP.
Beyond dipping patterns, DBP levels themselves are central to the classification of hypertension. Hypertension is broadly defined by a DBP of at least 90 mmHg, or by the use of antihypertensive medication.[1]More specific gradations exist, such as “moderate hypertension,” which may be characterized by a DBP of 95 mmHg or higher, or a history of antihypertensive medication use.[4]These clinical thresholds are essential for diagnosing and managing hypertension, providing a framework for interpreting DBP measurements and changes within the context of disease severity and treatment efficacy.
Key Terminology and Conceptual Frameworks
Section titled “Key Terminology and Conceptual Frameworks”Understanding the terminology associated with DBP is fundamental for accurate communication and research. “Diastolic Blood Pressure (DBP)” refers to the pressure in the arteries when the heart rests between beats, while “Ambulatory Blood Pressure (ABPM)” denotes the technique of measuring blood pressure at regular intervals outside of a clinical setting.[4] The terms “nocturnal dipping” and “night-to-day BP ratio” specifically describe the pattern and magnitude of DBP reduction during sleep, with a “non-dipper” denoting an insufficient nocturnal fall.[4] These terms are critical for characterizing the circadian rhythm of blood pressure.
Conceptual frameworks for DBP change extend beyond static measurements or simple day-night comparisons. “DBP trajectory” refers to the rate of DBP change over extended periods, often analyzed longitudinally to understand progression or regression of blood pressure.[1] The “blood pressure response” describes the alteration in DBP following interventions, such as the administration of antihypertensive medications.[5]Additionally, related concepts like “white coat syndrome,” where DBP readings are elevated in a clinical setting due to anxiety, highlight the importance of context.[7]Collectively, these terms and frameworks provide a comprehensive language for discussing, researching, and clinically evaluating the dynamic nature of diastolic blood pressure.
The Physiology of Diastolic Blood Pressure Dipping and its Cardiovascular Impact
Section titled “The Physiology of Diastolic Blood Pressure Dipping and its Cardiovascular Impact”Diastolic blood pressure (DBP) normally follows a diurnal pattern, typically decreasing during nighttime hours compared to daytime values, a phenomenon known as blood pressure dipping.[4]This natural rhythm is a crucial indicator of cardiovascular health, with international guidelines recommending ambulatory blood pressure (ABPM) to accurately assess nighttime DBP and its dipping status.[4]An attenuated or blunted nocturnal DBP dipping pattern is not merely a deviation from this rhythm; it is strongly associated with significant cardiovascular target organ damage and an increased risk for adverse cardiovascular events.[4]Studies have demonstrated that blunted nighttime blood pressure dipping in untreated hypertensive individuals independently predicts a variety of critical cardiovascular outcomes, including coronary events, strokes, cardiovascular deaths, and total mortality, irrespective of the overall 24-hour blood pressure levels.[4]This highlights the importance of DBP dipping as a prognostic marker, reflecting underlying pathophysiological processes that contribute to cardiovascular disease progression. The accurate assessment and understanding of DBP changes, particularly the nocturnal dipping pattern, are therefore essential for comprehensive cardiovascular risk stratification and management.
Molecular and Cellular Mechanisms of Blood Pressure Regulation
Section titled “Molecular and Cellular Mechanisms of Blood Pressure Regulation”The intricate regulation of diastolic blood pressure and its circadian rhythm involves a complex interplay of molecular and cellular pathways within the cardiovascular system. Key biomolecules, such as the Kv9.3 subunit encoded by the_KCNS3_gene, play a critical role as a component of voltage-gated potassium channels, which are essential for regulating the contraction of arterial smooth muscle cells.[4] Proper functioning of these channels is vital for maintaining vascular tone and resistance, directly influencing DBP levels. Disruptions in these cellular functions can lead to altered vascular responsiveness and contribute to blood pressure dysregulation.
Furthermore, the body’s internal clock, governed by core circadian genes like _BMAL1_, significantly influences the diurnal variation of blood pressure.[8] Animal studies have shown that mutations or deletions in these core circadian genes can disrupt the normal circadian rhythm of blood pressure, underscoring their importance in maintaining physiological dipping.[8], [9] Other genes, such as _ERAP2_, _GPR65_, and _SNX30_, also exhibit expression patterns that may be linked to blood pressure regulation, suggesting broader regulatory networks at play.[4] The _YY1_regulatory motif, for instance, shows increased expression in hypertensive elastic arteries, pointing to its potential role in the vascular remodeling associated with hypertension.[1]
Genetic Architecture and Regulatory Networks of Diastolic Blood Pressure
Section titled “Genetic Architecture and Regulatory Networks of Diastolic Blood Pressure”Genetic mechanisms contribute substantially to the variability in DBP dipping, with studies indicating that approximately 81% of the heritability in diastolic blood pressure dipping is attributable to genetic influences.[10]Genome-wide association studies (GWAS) have identified several genetic loci and single nucleotide polymorphisms (SNPs) associated with DBP and its dipping pattern. For example,*rs10817396 *has been linked to both systolic and diastolic blood pressure as well as sleep traits like chronotype and sleeplessness.[4] Similarly, *rs16984571 *, an intronic SNP within the _KCNS3_ gene, has also been associated with chronotype, further highlighting the genetic connections between circadian rhythms and blood pressure.[4] Specific SNPs can also act as expression quantitative trait loci (eQTLs), influencing the expression levels of nearby genes. For instance, *rs2119704 * is an eQTL for _GPR65_ expression, and *rs10817396 * is an eQTL for _SNX30_ expression in selected tissues.[4] Another variant, *rs4060030 *, has been associated with decreasing systolic blood pressure trajectory and also influences DBP trajectory, serving as an eQTL for_LOC101927039_ in the heart atrial appendage and binding to regulatory motifs such as _YY1_.[1] Other genes like _ATP2B1_, _CSK_, _ARSG_, _CSMD1_, _IGF1_, _SLC4A4_, _WWOX_, _SFMBT1_, and _HSD3B1_have also been implicated in blood pressure regulation or hypertension susceptibility, underscoring the polygenic nature of this complex trait.[11], [12], [13]
Pathophysiological Implications and Systemic Interactions
Section titled “Pathophysiological Implications and Systemic Interactions”The disruption of normal DBP dipping is not merely a genetic or molecular anomaly but manifests as significant pathophysiological processes with systemic consequences. The strong association between attenuated nocturnal DBP dipping and cardiovascular target organ damage, including coronary events, strokes, and cardiovascular deaths, underscores its role as a critical indicator of compromised cardiovascular health.[4] This blunted dipping is thought to reflect a homeostatic disruption where the body fails to adequately lower blood pressure during rest, leading to sustained vascular stress.
At the organ level, the sustained elevated nighttime DBP can contribute to conditions like left ventricular hypertrophy (LVH), a compensatory response where the heart muscle thickens due to increased workload.[4]Additionally, specific genetic loci associated with coronary artery disease (CAD) have also been linked to non-dipping status, indicating a shared genetic and mechanistic basis for these cardiovascular pathologies.[14] Genes such as _BCL11B_have been suggested to play a role in cardiovascular pathophysiology, and_C8orf37-AS1_has been associated with heart rate response to beta-blockers, illustrating the complex interplay between genetic factors, physiological processes, and therapeutic responses in blood pressure regulation and related cardiovascular conditions.[1], [4]
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Changes in diastolic blood pressure (DBP) are influenced by a complex interplay of genetic factors, signaling cascades, metabolic processes, and systemic regulatory mechanisms. These pathways integrate environmental cues with intrinsic physiological rhythms to maintain vascular homeostasis, and their dysregulation can contribute to conditions like hypertension. Understanding these underlying mechanisms is crucial for identifying therapeutic targets and predicting individual responses to treatments.
Circadian Rhythms and Vascular Contractility
Section titled “Circadian Rhythms and Vascular Contractility”The diurnal pattern of blood pressure, characterized by lower values at night (BP dipping), is a fundamental aspect of cardiovascular physiology, with attenuated nocturnal DBP dipping linked to increased cardiovascular risk.[15] This rhythm is significantly influenced by core circadian clock genes, such as BMAL1, which regulate the circadian variation of blood pressure by modulating gene expression in various tissues, including smooth muscle.[9] Genetic variations within genes like KCNS3, which codes for a subunit of voltage-gated potassium channels (Kv9.3), directly regulate the contraction of arterial smooth muscle, thereby influencing vascular tone and DBP. Polymorphisms inKCNS3 have been associated with chronotype, suggesting a link between an individual’s internal clock and vascular regulation.[4]
Neurohumoral Signaling and Ion Channel Modulation
Section titled “Neurohumoral Signaling and Ion Channel Modulation”Diastolic blood pressure is tightly controlled by neurohumoral pathways that regulate vascular smooth muscle contraction and relaxation. The rapid response to alpha-1 adrenergic agents, such as phenylephrine, highlights the role of adrenergic signaling in modulating vascular tone, a process impacted by individual genomics.[3] Nitric oxide (NO) signaling is another critical pathway, with nitric oxide synthases (NOS) regulating its production and function to promote vasodilation.[16] Neuronal nitric oxide synthase (NOS1) and its regulator NOS1AP modulate cardiac repolarization and vascular responses.[17]Furthermore, calcium handling within cells, crucial for muscle contraction, is influenced by proteins likeCAPON which modulates neuronal calcium and cardiac sympathetic neurotransmission, and calcium pumps like ATP2B1 which are directly related to blood pressure regulation.[18]
Genetic Regulatory Mechanisms and Metabolic Influences
Section titled “Genetic Regulatory Mechanisms and Metabolic Influences”Gene regulation plays a pivotal role in DBP changes, with expression quantitative trait loci (eQTLs) linking genetic variants to gene expression levels, thereby influencing downstream physiological processes. For instance, rs10044521 is an eQTL for ERAP2 (Endoplasmic Reticulum Aminopeptidase 2) expression, and rs2119704 and rs10817396 are eQTLs for GPR65 and SNX30 expression, respectively, in selected tissues.[4] These regulatory relationships can alter protein abundance and function, affecting DBP. Metabolic pathways also exert significant control; polymorphisms in genes like HSD3B1(3-beta-hydroxysteroid dehydrogenase type I) are associated with blood pressure, indicating a role for steroid hormone metabolism.[13] Additionally, genetic loci influencing circulating levels of phospholipids, including n-3 fatty acids and trans fatty acids, and other blood metabolites, underscore the broad metabolic context impacting DBP.[19]
Systems-Level Integration and Disease Relevance
Section titled “Systems-Level Integration and Disease Relevance”The regulation of DBP involves intricate pathway crosstalk and network interactions, where multiple genetic and environmental factors converge. For example, the insulin-like growth factor (IGF1) pathway, involving IGFBP-3, is crucial for vascular repair and nitric oxide generation, linking growth factor signaling to vascular health.[20]Dysregulation in these integrated systems can lead to hypertension; genes likeBCL11B, CSK, ARSG, CSMD1, SLC4A4, WWOX, SFMBT1, ATP1B1, RGS5, and SELEhave all been implicated as hypertension susceptibility genes or in BP regulation.[11] Understanding these interactions facilitates the identification of therapeutic targets and informs pharmacogenomic approaches, as demonstrated by studies on the genetic influences on blood pressure response to various antihypertensive drugs like hydrochlorothiazide.[21]
Prognostic Value and Cardiovascular Risk Stratification
Section titled “Prognostic Value and Cardiovascular Risk Stratification”Changes in diastolic blood pressure (DBP) over time, particularly the nocturnal dipping pattern, hold significant prognostic value for cardiovascular outcomes. A diminished nocturnal DBP fall, known as a “non-dipping” pattern, has been consistently identified as a predictor of increased risk of death and cardiovascular events in hypertensive patients.[22], [23] Understanding these dynamic changes through ambulatory blood pressure monitoring (ABPM) allows clinicians to identify high-risk individuals who may benefit from more intensive management or closer follow-up, thereby enhancing personalized medicine approaches and prevention strategies. Furthermore, the analysis of longitudinal DBP trajectories has been shown to uncover novel genetic associations and provide a more robust assessment of long-term risk compared to single cross-sectional measurements.[1]
Diagnostic Utility and Monitoring Strategies
Section titled “Diagnostic Utility and Monitoring Strategies”The of DBP change is crucial for comprehensive diagnostic assessment and effective monitoring of hypertension and related conditions. ABPM, which captures DBP values throughout day and night, is instrumental in characterizing the nocturnal DBP dipping pattern, defining the night-to-day DBP ratio, and providing mean DBP values over various periods.[4]This detailed information aids in diagnosing masked hypertension, white-coat hypertension, and identifying individuals with an adverse non-dipping pattern, which may otherwise be missed by office measurements. Ongoing monitoring of DBP trajectories helps clinicians track disease progression, evaluate the effectiveness of lifestyle interventions, and adjust therapeutic regimens to optimize long-term patient care.[1] In acute care settings, rapid DBP responses to pharmacological agents like phenylephrine are also monitored, providing immediate insights into hemodynamic status and guiding timely interventions.[3]
Therapeutic Response, Comorbidities, and Personalized Medicine
Section titled “Therapeutic Response, Comorbidities, and Personalized Medicine”Diastolic blood pressure changes are intimately linked with the development of comorbidities and the response to antihypertensive therapies, paving the way for personalized medicine approaches. A blunted nocturnal DBP dip is associated with target organ damage, such as left ventricular hypertrophy, in patients with essential hypertension.[15] Moreover, genetic factors play a significant role in modulating DBP changes and treatment efficacy; for instance, specific genetic variants like rs79237970 in WDR92 have been linked to differential DBP responses to various antihypertensive agents, including thiazide, metoprolol, and atenolol.[6] These genetic insights allow for tailoring drug selection based on an individual’s predicted response, enhancing treatment effectiveness and minimizing adverse effects. Studies have also shown that associations of DBP dipping with genetic markers remain consistent even during antihypertensive drug administration, highlighting the intrinsic nature of these patterns.[4]
Frequently Asked Questions About Diastolic Blood Pressure Change
Section titled “Frequently Asked Questions About Diastolic Blood Pressure Change”These questions address the most important and specific aspects of diastolic blood pressure change based on current genetic research.
1. Why does my blood pressure stay high even if I sleep enough?
Section titled “1. Why does my blood pressure stay high even if I sleep enough?”It’s possible your body doesn’t “dip” its blood pressure enough at night, even with good sleep. This nocturnal non-dipping can have a genetic component; for example, variations near genes like BCL11B have been linked to how much your blood pressure falls during sleep. Your circadian clock genes also play a role in regulating this natural nighttime drop.
2. Will my kids inherit my unusual nighttime blood pressure?
Section titled “2. Will my kids inherit my unusual nighttime blood pressure?”There’s a good chance they might, as genetics play a significant role in blood pressure patterns. Genome-wide association studies have identified many genetic variations, like those near GPR65 or SNX30, that are associated with how your blood pressure changes, especially at night. These genetic predispositions can be passed down.
3. Does my work stress actually mess with my blood pressure at night?
Section titled “3. Does my work stress actually mess with my blood pressure at night?”Yes, stress can certainly influence your blood pressure, partly through its impact on your autonomic nervous system, which helps regulate blood pressure. While the direct genetic links for stress specifically impacting nocturnal dipping aren’t fully detailed, your genes can influence how your body responds to various stimuli, including stress, affecting overall blood pressure regulation.
4. Does my family’s background change my blood pressure risk?
Section titled “4. Does my family’s background change my blood pressure risk?”Yes, your ancestral background can influence your blood pressure risk and patterns. Research has shown that genetic influences on blood pressure can differ across populations, meaning certain genetic factors might be more common or have different effects in specific ethnic groups. This highlights why it’s important to consider your background for a complete picture.
5. Why do my blood pressure pills not work as well as my friend’s?
Section titled “5. Why do my blood pressure pills not work as well as my friend’s?”Your genetic makeup can significantly influence how effective certain medications are for you. For instance, specific genetic variants, like one in the WDR92 gene, have been found to affect how individuals respond to common blood pressure medications like thiazide diuretics. This genetic difference can explain why a drug works better for one person than another.
6. Can I really fix my blood pressure patterns with just lifestyle changes?
Section titled “6. Can I really fix my blood pressure patterns with just lifestyle changes?”Lifestyle changes like diet and exercise are crucial, but genetics also play a role in your blood pressure patterns. While environmental factors influence DBP change, genetic factors also contribute to your predisposition for “dipping” or “non-dipping.” A combination of healthy habits and understanding your genetic tendencies offers the best approach for management.
7. Is there a test that can predict my future heart risks from blood pressure?
Section titled “7. Is there a test that can predict my future heart risks from blood pressure?”Yes, an ambulatory blood pressure monitor (ABPM) that measures your blood pressure frequently over 24 hours can reveal patterns, like non-dipping, that predict future cardiovascular risks. Identifying these patterns, which can have genetic underpinnings, allows for earlier and more targeted interventions to protect your heart.
8. My sibling’s blood pressure is fine, but mine isn’t; why are we different?
Section titled “8. My sibling’s blood pressure is fine, but mine isn’t; why are we different?”Even within the same family, individual genetic variations and unique environmental exposures can lead to different health outcomes. While you share many genes with your sibling, specific single nucleotide polymorphisms (SNPs) associated with blood pressure change can vary, making your patterns different from theirs.
9. Is it true my blood pressure can slowly get worse over years?
Section titled “9. Is it true my blood pressure can slowly get worse over years?”Yes, blood pressure can change over time, and some genetic variants are even linked to specific blood pressure “trajectories.” For example, a variant in the RNA gene C8orf37-AS1has been associated with a decreasing diastolic blood pressure trajectory, but other factors and genetics can also lead to a gradual increase or other changes over many years.
10. Could I have hidden high blood pressure even if my doctor’s reading is normal?
Section titled “10. Could I have hidden high blood pressure even if my doctor’s reading is normal?”Absolutely. Your blood pressure can behave differently outside the doctor’s office, especially at night. If your blood pressure doesn’t drop enough during sleep (non-dipping), it can indicate hidden issues and increased cardiovascular risk, even if your daytime office readings are normal. An ABPM can reveal these crucial nocturnal patterns.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
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[2] Nandakumar, P. et al. “Rare coding variants associated with blood pressure variation in 15 914 individuals of African ancestry.” J Hypertens, vol. 35, no. 5, 2017, pp. 981-987.
[3] Wenric, S., et al. “Rapid response to the alpha-1 adrenergic agent phenylephrine in the perioperative period is impacted by genomics and ancestry.” Pharmacogenomics J, vol. 20, 2020, pp. 883–90.
[4] Rimpela, J. M. et al. “Genome-wide association study of nocturnal blood pressure dipping in hypertensive patients.” BMC Med Genet, vol. 19, no. 1, 2018, p. 114.
[5] Salvi, E. et al. “Genome-Wide and Gene-Based Meta-Analyses Identify Novel Loci Influencing Blood Pressure Response to Hydrochlorothiazide.” Hypertension, vol. 68, no. 1, 2016, pp. 131-40.
[6] Singh, S. et al. “Genome Wide Analysis Approach Suggests Chromosome 2 Locus to be Associated with Thiazide and Thiazide Like-Diuretics Blood Pressure Response.” Sci Rep, vol. 9, no. 1, 2019, p. 17351.
[7] Hendry, L. M. et al. “Insights into the genetics of blood pressure in black South African individuals: the Birth to Twenty cohort.”BMC Med Genomics, vol. 11, no. 1, 2018, p. 11.
[8] Xie, Z., et al. “Smooth-muscle BMAL1 participates in blood pressure circadian rhythm regulation.”J Clin Invest, vol. 125, no. 1, 2015, pp. 324–36.
[9] Curtis, A. M., et al. “Circadian variation of blood pressure and the vascular response to asynchronous stress.” Proc Natl Acad Sci U S A, vol. 104, no. 9, 2007, pp. 3450–5.
[10] Wang, X., et al. “Genetic influences on daytime and night-time blood pressure: similarities and differences.” J Hypertens, vol. 27, no. 12, 2009, pp. 2358–64.
[11] Hong, K-W., et al. “Genetic variations in ATP2B1, CSK, ARSG and CSMD1 loci are related to blood pressure and/or hypertension in two Korean cohorts.”Journal of Human Hypertension, vol. 24, no. 6, 2010, pp. 367–72.
[12] Yang, H-C., et al. “Identification of IGF1, SLC4A4, WWOX, and SFMBT1 as hypertension susceptibility genes in Han Chinese with a genome-wide gene-based association study.”PLoS ONE, vol. 7, no. 3, 2012, e32907.
[13] Rosmond, R., et al. “Polymorphism in exon 4 of the human 3 beta-hydroxysteroid dehydrogenase type I gene (HSD3B1) and blood pressure.” Biochem Biophys Res Commun, vol. 293, no. 1, 2002, pp. 629–32.
[14] Wirtwein, M., et al. “The relationship between gene polymorphisms and dipping profile in patients with coronary heart disease.”Am J Hypertens, vol. 29, no. 9, 2016, pp. 1094–102.
[15] Verdecchia, P., et al. “Circadian blood pressure changes and left ventricular hypertrophy in essential hypertension.”Circulation, vol. 81, 1990, pp. 528–36.
[16] Hermann, M., et al. “Nitric oxide in hypertension.”Journal of Clinical Hypertension, vol. 8, no. 1, 2006, pp. 17–29.
[17] Arking, D. E., et al. “A common genetic variant in the NOS1 regulator NOS1AP modulates cardiac repolarization.” Nature Genetics, vol. 38, no. 6, 2006, pp. 644–51.
[18] C-J L, et al. “CAPON modulates neuronal calcium handling and cardiac sympathetic neurotransmission during dysautonomia in hypertension.”Hypertension, vol. 65, no. 6, 2015, pp. 1288–97.
[19] Lemaitre, R. N., et al. “Genetic loci associated with plasma phospholipid n-3 fatty acids: a meta-analysis of genome-wide association studies from the CHARGE consortium.” PLoS Genetics, vol. 7, no. 7, 2011, e1002193.
[20] Kaplan, R. C., et al. “A genome-wide association study identifies novel loci associated with circulating IGF-I and IGFBP-3.” Human Molecular Genetics, vol. 20, no. 6, 2011, pp. 1241–51.
[21] Hiltunen, T. P., et al. “Pharmacogenomics of hypertension: a genome-wide, placebo-controlled cross-over study, using four classes of antihypertensive drugs.”Journal of the American Heart Association, vol. 4, no. 1, 2015, e001521.
[22] Fagard, R. H., et al. “Night-day blood pressure ratio and dipping pattern as predictors of death and cardiovascular events in hypertension.”J Hum Hypertens, vol. 23, 2009, pp. 645–53.
[23] Salles, G. F., et al. “Prognostic effect of the nocturnal blood pressure fall in hypertensive patients: the ambulatory blood pressure collaboration in patients with hypertension (ABC-H) meta-analysis.”Hypertension, vol. 67, 2016, pp. 693–700.