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Cardiology and Angiology

Cite as: Archiv EuroMedica. 2026. 16; 4. DOI 10.35630/2026/16/Iss.4.12

Received 14 July 2026;
Accepted 10 August 2026;
Published 15 August 2026

SLEEP DISORDERS AND HYPERTENSION: PATHOPHYSIOLOGICAL MECHANISMS, EPIDEMIOLOGICAL EVIDENCE AND CLINICAL IMPLICATIONS

Ewa Dapkiewicz1 orcid, Dawid Gąsowski2 orcid,
Sylwia Haba6 orcid, Katarzyna Łysynkiewicz3 email orcid,
Zuzanna Wątek3 orcid, Patrycja Krawczyk4 orcid,
Izabela Grzyb5 orcid, Jan Szewczyk5 orcid,
Alicja Smolińska5 orcid, Maria Bołoz3 orcid

1 Independent Public Health Care Facility of the Ministry of the Interior and Administration in Białystok, named after Marian Zyndram-Kościałkowski, Białystok, Poland
2 Independent Public Health Care Facility in Łapy, Poland
3 Jędrzej Śniadecki Regional Hospital, Białystok, Poland
4 Voivodeship Regional Hospital in Kielce, Poland
5 Polish Red Cross Maritime Hospital, Gdynia, Poland
6 University Clinical Hospital of Bialystok, Poland

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  kstepaniuk12@gmail.com

ABSTRACT

Background

Hypertension remains a major global health challenge and an important risk factor for cardiovascular disease. Increasing evidence indicates that sleep disorders and adverse sleep patterns are associated with blood pressure dysregulation and may contribute to the development or persistence of hypertension.

Aim

This narrative review aimed to evaluate the pathophysiological mechanisms, epidemiological evidence, and clinical implications of the relationship between sleep disorders and hypertension, with particular attention to poorly controlled and resistant hypertension.

Materials and Methods

A narrative literature review was conducted using PubMed/MEDLINE and Google Scholar from database inception to March 2026. Human observational and interventional studies, systematic reviews, meta-analyses, narrative reviews, and relevant clinical guidelines or position statements were included. A total of 149 publications were included in the narrative synthesis.

Results

Sleep disorders and adverse sleep patterns are associated with blood pressure dysregulation through sympathetic nervous system activation, impaired nocturnal blood pressure dipping, activation of the hypothalamic-pituitary-adrenal and renin-angiotensin-aldosterone systems, endothelial dysfunction, inflammation, oxidative stress, and, in obstructive sleep apnea, recurrent intermittent hypoxia. The strongest and most consistent evidence concerns obstructive sleep apnea, particularly in patients with resistant or poorly controlled hypertension. Short sleep duration, insomnia accompanied by objectively reduced sleep, and circadian disruption are also associated with hypertension, although the evidence is less consistent. Findings regarding restless legs syndrome and periodic limb movements during sleep remain heterogeneous.

Conclusions

Sleep disorders and adverse sleep patterns may contribute to impaired blood pressure regulation. Obstructive sleep apnea has the strongest documented association with hypertension, especially in patients with resistant or poorly controlled hypertension. Evidence for short sleep duration, insomnia with objectively reduced sleep, and circadian disruption is less consistent, while findings for restless legs syndrome and periodic limb movements during sleep remain heterogeneous. Assessment of sleep disorders and sleep patterns may help identify potentially modifiable factors contributing to inadequate blood pressure control.

Keywords: sleep disorders, blood pressure, hypertension, cardiovascular disease, obstructive sleep apnea, circadian rhythm, sympathetic nervous system

1. INTRODUCTION

Hypertension remains one of the most significant public health challenges worldwide and a major risk factor for cardiovascular diseases, including coronary artery disease, heart failure, and stroke. It is estimated to affect approximately 1.4 billion people globally, while only about one in five individuals achieves adequate blood pressure control despite the availability of a wide range of pharmacological and non-pharmacological treatment options. [1]

This highlights the need for a more precise understanding of the factors involved in the development and persistence of hypertension. In recent years, particular attention has been paid to the role of sleep in cardiovascular regulation [2, 3]. Physiologically restorative sleep is characterized by adequate duration, continuity, regularity, and alignment with circadian rhythms [4, 5]. It contributes to the maintenance of homeostasis through modulation of autonomic nervous system activity, metabolic processes, endocrine regulation, and endothelial function [2].

Sleep disorders constitute a heterogeneous group of conditions, including insomnia, obstructive sleep apnea, circadian rhythm disturbances, and restless legs syndrome. Their association with hypertension may involve distinct but partially overlapping mechanisms, including activation of the sympathetic nervous system and the hypothalamic pituitary adrenal axis, disruption of circadian blood pressure regulation, systemic inflammation, oxidative stress, and endothelial dysfunction. The relative contribution and clinical significance of these mechanisms differ according to the specific sleep disorder.

Accumulating epidemiological and clinical evidence indicates that sleep fragmentation, insufficient sleep duration, obstructive sleep apnea, and circadian misalignment are associated with elevated blood pressure and an increased risk of hypertension. The evidence is strongest for obstructive sleep apnea, whereas for other sleep disorders the causal nature of these associations remains less certain. Differences in study design, methods of sleep assessment, definitions of hypertension, and adjustment for confounding factors further limit direct comparison of the findings [2, 3, 4, 6, 7, 8, 9, 10, 11, 12].

Understanding these associations is clinically important, since sleep disorders represent a potentially modifiable risk factor, and their diagnosis and treatment may improve blood pressure control and decrease cardiovascular risk. Therefore, the evaluation of sleep habits and the occurrence of related disorders can be used in risk assessment and contribute to optimizing antihypertensive treatment, especially among patients with resistant or poorly controlled hypertension.

Although numerous studies have examined the relationship between sleep and hypertension, the available evidence remains heterogeneous. The strength of the reported associations differs across obstructive sleep apnea, short sleep duration, insomnia, restless legs syndrome, periodic limb movements during sleep, and circadian rhythm disruption. In addition, differences in study design, methods of sleep assessment, definitions of hypertension, and adjustment for confounding factors limit direct comparison of the findings. The novelty of this review lies in the integrated comparison of the main sleep related conditions, their underlying pathophysiological mechanisms, epidemiological evidence, and clinical relevance to hypertension within a single analytical framework.

The aim of this review is to critically evaluate current evidence on the relationship between sleep disorders and hypertension. The objectives are to analyze the principal pathophysiological mechanisms linking sleep disturbances with blood pressure dysregulation, compare epidemiological findings for individual sleep related conditions, and assess their clinical significance for identifying patients at increased risk and for the management of poorly controlled or resistant hypertension.

2. MATERIALS AND METHODS

This narrative review was based on a literature search conducted in PubMed/MEDLINE and Google Scholar from database inception to March 2026. The search strategy used the following Boolean combination: ((“sleep disorders” OR “sleep duration” OR insomnia OR “obstructive sleep apnea” OR “circadian rhythm” OR “shift work” OR “restless legs syndrome” OR “periodic limb movements”) AND (hypertension OR “blood pressure” OR “resistant hypertension”)).

Eligible sources included peer reviewed human observational and interventional studies, systematic reviews, meta analyses, narrative reviews, and relevant clinical guidelines or position statements addressing the epidemiology, pathophysiological mechanisms, or clinical implications of sleep disorders in hypertension.

Duplicate publications, conference abstracts, case reports, editorials without substantive evidence, animal and in vitro studies, and publications unrelated to the aim of the review were excluded.

Titles and abstracts were screened first, followed by full-text assessment. A total of 149 eligible publications, published between 1993 and March 2026, were identified and included in the narrative synthesis. For the tabular synthesis, representative studies were selected to cover each major sleep-related exposure, with priority given to meta-analyses, large cohort studies, and investigations reporting quantitative effect estimates.

3. RESULTS

3.1. Sleep Physiology and Blood Pressure Regulation

Sleep is crucial for cardiovascular regulation, as it affects autonomic nervous system activity, endocrine function, endothelial function, and the circadian rhythm of blood pressure. [13, 14] During normal sleep, blood pressure decreases by approximately 10–20% for systolic values and slightly less for diastolic values. This is referred to as nocturnal “dipping,” with blood pressure gradually increasing toward the end of sleep and rising sharply upon awakening. [15-16]

During sleep, sympathetic nervous system activity decreases while parasympathetic activity predominates, leading to a reduced heart rate, peripheral resistance, and blood pressure. However, transient blood pressure fluctuations may also occur. Additionally, physiological changes associated with the sleep-wake cycle, such as body position and reduced physical activity, can mask or modify blood pressure fluctuations regulated by endogenous circadian mechanisms. A mismatch between local biological clocks supporting nocturnal recovery and persistent cardiovascular activity may contribute to the increased cardiovascular risk associated with elevated nighttime blood pressure. [17]

One of the key mechanisms linking sleep disorders to hypertension is chronic activation of the sympathetic nervous system. Sleep fragmentation, frequent arousals, and reduced total sleep duration increase sympathetic activity at night and during the day, elevating heart rate, increasing vascular resistance, and sustaining elevated blood pressure. [16] Sleep disturbances, including insomnia, shift work, and obstructive sleep apnea, may lead to a blunting or loss of the nocturnal blood pressure decline, a pattern referred to as a “non-dipper” profile. [17] This profile is associated with an increased risk of cardiovascular complications, such as left ventricular hypertrophy, stroke, and coronary artery disease. [19,20] Studies have demonstrated that sleep traits, including reduced sleep duration and increased sleep fragmentation, are associated with a non-dipper blood pressure profile, even in normotensive individuals. [21]

Sleep disturbances also affect hormonal balance. Insufficient sleep can significantly enhance hypothalamic-pituitary-adrenal axis reactivity to stress, leading to increased cortisol secretion. Shortened and fragmented sleep additionally activate the renin-angiotensin-aldosterone system, leading to sodium retention, increased blood volume, and elevated blood pressure. [22]

Melatonin is synthesized in darkness, and its concentration increases during nocturnal sleep. [15] Nocturnal melatonin secretion has been shown to increase nitric oxide production and reduce norepinephrine levels, thereby promoting vasodilation and supporting endothelial function. [23] Consequently, lower melatonin secretion may be associated with impaired vasodilation and higher nocturnal blood pressure.

3.2. Epidemiology of Sleep Disorders and Hypertension

Sleep disorders constitute a common health problem of significant epidemiological importance. It is estimated that over 30% of adults in the United States experience insufficient sleep (<7 hours). [24] Data from the representative NHANES (National Health and Nutrition Examination Survey), including over 12,000 adults aged 30–79 years, showed that the prevalence of hypertension was 37.8%, and individuals with short sleep duration (<7 hours) or sleep disturbances had a significantly higher risk of hypertension compared to those with a “healthy” sleep pattern (OR = 1.20–1.45). [24] Similar associations were also observed in analyses of NHANES 2005–2008 data, where coexisting sleep disturbances and short sleep duration were associated with a higher likelihood of hypertension, and the combination of multiple sleep characteristics further amplified this effect. [3]

Obstructive sleep apnea is the most extensively studied sleep disorder associated with hypertension, with the risk increasing alongside disease severity and being particularly high among patients with resistant hypertension. [12,25–27] Insomnia, especially when accompanied by short sleep duration, and insufficient sleep itself have also been associated with an increased risk of hypertension. [28-29, 100, 102-104] Disruption of circadian rhythms, particularly in shift workers, is linked to elevated blood pressure, while restless legs syndrome, poor sleep quality, and sleep fragmentation appear to show more modest and less consistent associations. [24,28,30-31] These relationships are discussed in greater detail in the following sections.

3.3. Impact of Obstructive Sleep Apnea on the Risk of Hypertension

Obstructive sleep apnea (OSA) is one of the most well-documented sleep disorders associated with the development of hypertension. This condition is characterized by recurrent episodes of upper airway obstruction during sleep, leading to intermittent hypoxia, sleep fragmentation, and fluctuations in intrathoracic pressure. Obesity is the primary risk factor for OSA; however, other factors such as age, male sex, anatomical abnormalities, allergies, alcohol consumption, smoking, and the use of sedative medications also contribute to its development. [32-37] It is important to emphasize that obesity, as a major risk factor for OSA, is itself independently associated with an increased risk of hypertension. [38-41]

A key mechanism linking OSA with hypertension is increased sympathetic nervous system activity, driven by recurrent arousals from sleep, activation of arterial chemoreceptors, and enhanced arterial chemoreflex sensitivity, as well as upregulation of the renin-angiotensin-aldosterone system, promoting fluid retention. Furthermore, intermittent hypoxia contributes to sympathetic overactivity, increases oxidative stress, and enhances systemic inflammation. OSA is also associated with endothelial dysfunction, partly due to reduced nitric oxide synthase activity and increased endothelin-1 levels, a potent vasoconstrictor and mitogen. OSA-related disturbances in autonomic regulation and hormonal balance contribute to the development of insulin resistance, increased platelet activation, hyperleptinemia, and impaired renal function, further elevating cardiovascular risk. Additionally, attention has been drawn to the role of increased cyclooxygenase activity, which may further promote atherosclerosis and contribute to adverse cardiovascular outcomes. [17,34,42-48]

Epidemiological studies, prospective cohorts, and meta-analyses consistently demonstrate a severity-dependent association between OSA and hypertension. The relationship is particularly strong for resistant hypertension, in which OSA is highly prevalent and is associated with poorer nocturnal blood pressure control. Representative quantitative findings are summarized in Table 1 [25,49-60].

Furthermore, increasing attention has been paid to the potential risks associated with obstructive sleep apnea in pregnant women, as it may significantly contribute to the development of pregnancy-related complications and adversely affect both maternal and fetal health. [61-65] An analysis including 1,577,632 pregnant women showed that those with OSA are at a higher risk of pregnancy-specific complications, particularly hypertensive disorders of pregnancy. After adjusting for potential confounders, OSA remained significantly associated with an increased risk of preeclampsia (OR = 2.22; 95% CI 1.94-2.54) and eclampsia (OR = 2.95; 95% CI 1.08-8.02). [61]

Management of obstructive sleep apnea is considered an important factor in reducing hypertension risk and improving blood pressure control. Continuous Positive Airway Pressure (CPAP) therapy is particularly important, as it maintains upper airway patency, preventing episodes of hypopnea and apnea. [66-67] In addition to keeping airway patency, CPAP therapy has been shown to reduce sympathetic nervous system activity, suppress the renin-angiotensin-aldosterone system, and decrease oxidative stress. These effects result in a lower blood pressure and improved endothelial function. Evidence obtained from multiple studies indicates that CPAP treatment may modestly reduce blood pressure, particularly in patients with resistant hypertension and adequate treatment adherence; however, evidence for a reduction in major cardiovascular events remains less consistent. [68-75]

3.4. Impact of Sleep Duration on the Risk of Hypertension

When discussing sleep disturbances and their relationship with the development of hypertension, sleep duration, particularly insufficient sleep, also represents an important factor. Nowadays, sleep restriction is widespread, often associated with lifestyle choices, career demands, and stress. [76-78]

Large cohort studies and meta-analyses generally associate short sleep duration with a higher risk of prevalent and incident hypertension. The strength of this relationship varies according to the sleep-duration threshold, age, and sex. Evidence regarding long sleep duration is less consistent, with some analyses suggesting a U-shaped association and others showing no statistically significant increase in incident hypertension. Representative estimates are presented in Table 1 [6,29,80,88-91].

On the other hand, some studies have not found a significant relationship between sleep duration and hypertension. [84,85]

The pathogenesis of hypertension resulting from short sleep duration is thought to involve hyperactivation of the hypothalamic-pituitary-adrenal axis, accompanied by increased sympathetic nervous system activity and enhanced renal sodium retention. [92-93] Available evidence highlights the need for comprehensive analyses to better understand the complexity of factors influencing sleep duration and their interactions. It is particularly important to consider gender and age differences, which can significantly modify the impact of sleep duration on the risk of hypertension. It is also important to emphasize the role of lifestyle, including physical activity, diet, and exposure to stress, which can modulate the described relationships.

3.5. Impact of Insomnia on the Risk of Hypertension

Insomnia is a sleep disorder characterized by difficulty initiating sleep, maintaining sleep, or experiencing early morning awakenings, accompanied by impaired daytime functioning, such as fatigue, reduced concentration, and irritability. Insomnia may be short-term (acute) or chronic; chronic insomnia is diagnosed when symptoms persist for at least three months and occur at least three times per week. [94] Contemporary data confirm the existence of the phenotype known as “insomnia with objective short sleep duration,” which is associated with the highest cardiovascular risk. It is believed to be driven by a state of chronic hyperarousal, involving increased activity of the sympathetic nervous system as well as the hypothalamic–pituitary–adrenal axis. [2,95-96] This leads to increased cortisol secretion, elevated vascular resistance, and impaired regulation of blood pressure. [97-98] The production of proinflammatory cytokines also plays a significant role in the pathomechanism of insomnia, increasing oxidative stress, leading to endothelial damage and impaired vasodilation. [96,97] From a clinical perspective, the heterogeneity of insomnia is important. Patients with subjective symptoms despite normal sleep duration may not exhibit an increased risk of hypertension, whereas individuals with objectively short sleep duration constitute a high-risk group. [98-99] Previous studies suggested an inconsistent association between insomnia symptoms and blood pressure levels, which was partly attributable to the lack of an objective assessment of sleep duration. [100]

The available evidence indicates that the cardiovascular significance of insomnia depends partly on objectively measured sleep duration. Chronic insomnia accompanied by short sleep is associated with a substantially higher hypertension risk, whereas insomnia without reduced sleep duration shows weaker or non-significant associations. Meta-analyses nevertheless suggest a modest overall increase in risk, particularly for impaired sleep maintenance and early morning awakening. Representative findings are summarized in Table 1 [98-104].

In summary, insomnia, particularly when combined with short sleep duration, represents a significant and potentially modifiable risk factor for hypertension that should be considered in cardiovascular risk assessment. [99]

3.6. Impact of Restless Legs Syndrome and Periodic Limb Movements during Sleep on the Risk of Hypertension

Restless legs syndrome (RLS) is a neurological disorder characterized by unpleasant sensorimotor sensations in the lower limbs. Symptoms typically occur at rest and are most pronounced in the evening and at night, leading to an urge to move the legs or get out of bed, which disrupts sleep continuity and overall rest. These disturbances may extend into the early morning hours. [106-107] RLS is a clinical syndrome diagnosed on the basis of symptoms, whereas periodic limb movements during sleep (PLMS) are objectively recorded, repetitive limb movements occurring during sleep.

Studies assessing RLS as a clinical syndrome, including population-based studies and meta-analyses, generally suggest a modest association between RLS and the presence of hypertension, with stronger relationships reported for frequent symptoms and secondary RLS. However, several studies found no statistically significant association, indicating substantial heterogeneity across populations and measurement methods. Representative findings are shown in Table 1. [31,108-119]

Periodic limb movements during sleep have been examined separately as a possible mechanism contributing to transient nocturnal elevations in blood pressure. PLMS-related sleep fragmentation and microarousals may increase sympathetic activity and disrupt autonomic balance, elevating heart rate and blood pressure during sleep. [110,120-124] Repeated nocturnal surges in blood pressure and heart rate may increase cardiovascular risk by enhancing oxidative stress and systemic inflammation, which may contribute to the development of cardiovascular diseases, including atherosclerosis. [125] Additionally, inflammation is associated with endothelial dysfunction and activation of the renin-angiotensin-aldosterone system, which may facilitate the onset and progression of hypertension. [126]

In a study by Trotti et al., 137 patients with restless legs syndrome were assessed for periodic limb movements during sleep, and plasma inflammatory markers such as CRP, IL-6, and TNF-α were measured. The results demonstrated that patients with RLS who exhibited a higher frequency of PLMS (≥45 per hour) had elevated CRP levels (OR = 3.56; 95% CI 1.26-10.03; P = 0.02; df = 1). After adjusting for confounding factors, including CRP-lowering medications, hyperlipidemia, inflammatory diseases, diabetes, and hypertension, the association remained significant (OR = 8.60; 95% CI 1.23-60.17; P = 0.03; df = 10). [127] Similarly, Bekci et al. observed that elevated levels of CRP and Lp-PLA2 were associated with increased numbers of PLMS, suggesting a potential increase in cardiovascular risk among these patients. [128] Previous studies by Benediktsdottir et al. and Berger et al. indicated that elevated CRP levels are not directly related to the mere presence of RLS. [117,129] However, the association between PLMS and inflammatory markers alone should not be interpreted as evidence that PLMS have a causal role in the development of hypertension.

Despite the growing number of studies on restless legs syndrome and periodic limb movements during sleep, significant uncertainties remain regarding the underlying pathomechanisms and their impact on overall body functioning. Therefore, further research is needed, including appropriately designed methodology that considers proper subject selection, standardized measurement and data collection methods, as well as potential confounding factors.

3.7. Impact of Circadian Rhythm Disruption on the Risk of Hypertension

Another factor contributing to the risk of developing hypertension is disruption of the circadian rhythm, which is particularly evident among shift workers. [30,130-139] Night work desynchronizes the circadian system, which consists of the central pacemaker in the suprachiasmatic nucleus of the hypothalamus and peripheral oscillators located in organs, tissues, and cells throughout the body. This system, through regulation of clock gene expression, coordinates and maintains 24-hour physiological rhythms, including blood pressure patterns. Disruption of these rhythms leads to a loss of the physiological nocturnal blood pressure dip and an increase in mean 24-hour blood pressure. [132]

Controlled circadian-misalignment experiments demonstrate small but measurable increases in 24-hour blood pressure, attenuation of nocturnal dipping, altered catecholamine and cortisol rhythms, and reduced parasympathetic activity. These findings provide direct physiological support for the epidemiological association between shift work, circadian disruption, and hypertension. Representative experimental results are summarized in Table 1 [140-141].

An important mechanism linking circadian rhythm disruption with impaired blood pressure regulation is abnormal melatonin secretion. [147-148] Nighttime exposure to light suppresses melatonin secretion and may impair melatonin receptor function, disrupting circadian rhythms, and contributing to poorer sleep quality and an increased risk of cardiovascular disorders. [138] Melatonin exerts multifaceted cardiovascular effects, including inhibition of sympathetic activity, vasodilatation, improvement of endothelial function, favorable modulation of lipid profiles, reduction of oxidative stress, and anti-inflammatory actions, collectively promoting cardiovascular regulation and protection. [146-148]

Shift work further leads to abnormal cortisol secretion patterns, including flattened peaks, delayed response, and overall hormonal dysregulation, which can affect metabolism, immune function, and stress responses, thereby increasing the risk of developing cardiovascular disease. These disruptions also enhance sympathetic activity. [148-149]

Moreover, endothelial dysfunction, increased arterial stiffness, and alterations in renal sodium metabolism may contribute to the development of hypertension. Shift work may also compromise sleep quality, causing fragmentation and irregular sleep timing, which challenge physiological adaptation to work schedules. [146] A consolidated overview of representative studies evaluating the relationships between major sleep-related factors and hypertension is presented in Table 1.

Table 1. Summary of representative studies and meta-analyses evaluating associations between sleep-related factors and hypertension.

Author, year [reference]Study design and populationSleep-related exposureKey quantitative findings
Peppard et al., 2000 [25]Prospective cohort; 709 participants from the Wisconsin Sleep Cohort; 4-year follow-upSleep-disordered breathing assessed with AHICompared with an AHI of 0 events/hour, the odds of hypertension at follow-up increased with baseline AHI: OR 1.42 for AHI 0.1–4.9, OR 2.03 for AHI 5.0–14.9, and OR 2.89 for AHI ≥15 events/hour.
Hou et al., 2018 [52]Systematic review and meta-analysis; 26 studies, 51,623 participantsOSA severity and resistant hypertensionHypertension risk increased with OSA severity: OR 1.184 for mild, 1.316 for moderate, and 1.561 for severe OSA; resistant hypertension OR 2.842.
Sapina-Beltran et al., 2019 [57]Observational study; 284 patients with resistant hypertensionOSA prevalence and severityOSA prevalence was 83.5%; increasing OSA severity was associated with higher blood pressure, particularly during the night.
Bourjeily et al., 2017 [61]National cohort; 1,577,632 pregnant womenOSA during pregnancyOSA was associated with preeclampsia (adjusted OR 2.22; 95% CI 1.94-2.54) and eclampsia (adjusted OR 2.95; 95% CI 1.08-8.02).
Hosseini et al., 2024 [6]Systematic review and meta-analysis; 16 cohort studiesShort and long sleep durationShort sleep was associated with incident hypertension (HR 1.07; 95% CI 1.06-1.09), with a stronger association for <=5 hours (HR 1.11); long sleep was not significant.
Grandner et al., 2018 [91]Cross-sectional analysis; more than 700,000 adultsSelf-reported sleep durationCompared with 7 hours, hypertension odds were higher for <=4 hours (OR 1.86), 5 hours (OR 1.56), 6 hours (OR 1.27), 9 hours (OR 1.19), and >=10 hours (OR 1.41).
Fernandez-Mendoza et al., 2012 [102]Population-based Penn State cohort; chronic insomnia evaluated with objective sleep durationInsomnia with objectively short sleepChronic insomnia with sleep duration <6 hours was associated with incident hypertension (OR 3.8), supporting a high-risk physiological insomnia phenotype.
Shen et al., 2018 [108]Meta-analysis; 9 population-based studiesRestless legs syndromeRLS was associated with a higher prevalence of hypertension (OR 1.36; 95% CI 1.18-1.57).
Giannini et al., 2014 [116]Population-based study; 1,709 participantsRestless legs syndromeNo statistically significant association with hypertension was observed (OR 1.20; 95% CI 0.85-1.80).
Scheer et al., 2009 [140]Controlled forced-desynchrony experiment in healthy adultsCircadian misalignmentCircadian misalignment increased mean awake blood pressure by approximately 3 mmHg (P<0.001) and altered cortisol and adrenaline rhythms.
Morris et al., 2016 [141]Controlled crossover protocol; two 8-day laboratory conditionsBehavioral and circadian misalignmentMean 24-hour systolic and diastolic blood pressure increased by 3.0 and 1.5 mmHg, and the nocturnal systolic dip decreased by 21%.

Abbreviations: AHI, apnea-hypopnea index; CI, confidence interval; HR, hazard ratio; OR, odds ratio; OSA, obstructive sleep apnea; RLS, restless legs syndrome.

As shown in Table 1, the selected studies demonstrate a dose-response relationship between OSA severity and hypertension, consistent associations between short sleep and elevated hypertension risk, a particularly strong association for insomnia combined with objective short sleep, heterogeneous findings for RLS, and experimentally measurable blood pressure increases during circadian misalignment.

4. DISCUSSION

The present review indicates that sleep-related disturbances do not contribute equally to hypertension risk. The most consistent evidence concerns obstructive sleep apnea, for which prospective cohorts, population-based studies, and meta-analyses demonstrate dose-response relationships with both incident and resistant hypertension [25,49-60]. Short sleep duration is also repeatedly associated with hypertension, although the magnitude of the effect is generally smaller and appears to vary with age, sex, and the threshold used to define insufficient sleep [6,29,80,86-91]. In insomnia, the clearest cardiovascular signal is observed when symptoms coexist with objectively short sleep, suggesting that physiological hyperarousal and reduced sleep duration identify a clinically important high-risk phenotype [98-104]. By contrast, findings for restless legs syndrome are less uniform, while experimental circadian-misalignment studies provide direct evidence that disruption of sleep timing can increase blood pressure and attenuate nocturnal dipping [108,114-119,140-141].

The convergence of these findings is biologically plausible because the analyzed sleep disturbances share several pathophysiological pathways. Recurrent arousals, sleep fragmentation, intermittent hypoxia, and insufficient sleep promote sympathetic activation, hypothalamic-pituitary-adrenal axis stimulation, renin-angiotensin-aldosterone system activity, oxidative stress, systemic inflammation, and endothelial dysfunction [2,16-23,34,42-48,92,93,95-98]. These mechanisms can increase vascular resistance, sodium retention, and circulating blood volume, while simultaneously impairing nitric oxide-dependent vasodilatation. They also favor a non-dipping or nocturnal-hypertension phenotype, which is clinically important because nighttime blood pressure provides prognostic information beyond daytime measurements [17-21]. OSA may generate the strongest association because intermittent hypoxia and repeated intrathoracic pressure changes act in addition to the mechanisms shared with other sleep disorders.

Differences between studies should be interpreted in the context of methodological heterogeneity. Sleep duration and insomnia are frequently assessed by self-report, whereas objective methods such as polysomnography or actigraphy may identify different risk groups. This distinction may explain why insomnia without objectively short sleep is inconsistently associated with hypertension. Similarly, the reported relationship between long sleep and hypertension may reflect reverse causation or confounding by age, chronic disease, reduced physical activity, depression, and medication use rather than a direct effect of prolonged sleep. In RLS, inconsistent results may arise from differences in symptom frequency, primary versus secondary disease, the presence of periodic limb movements, and adjustment for cardiovascular and metabolic comorbidities [108,114-119]. Consequently, the strength of causal inference is greater for OSA and experimentally induced circadian misalignment than for associations based solely on cross-sectional or questionnaire-derived data.

The findings have practical implications for hypertension assessment. Patients with resistant, nocturnal, or poorly controlled hypertension should be evaluated for OSA, particularly when obesity, snoring, witnessed apneas, or daytime sleepiness are present [12,27,53-60]. A routine sleep history should also address sleep duration, insomnia symptoms, shift-work exposure, and irregular sleep timing. Ambulatory blood pressure monitoring may be particularly useful when sleep disruption or a non-dipping pattern is suspected. Treatment of OSA with continuous positive airway pressure can improve endothelial and autonomic function and may reduce blood pressure, especially in patients with severe OSA, resistant hypertension, and good treatment adherence [66-75]. Nevertheless, sleep-focused interventions should complement rather than replace established antihypertensive treatment and management of obesity, diet, physical inactivity, alcohol consumption, and other cardiovascular risk factors.

Future research should use standardized definitions of sleep disturbances and hypertension, objective sleep assessment, and 24 hour ambulatory blood pressure monitoring. Prospective studies should evaluate the combined effects of sleep duration, continuity, timing, regularity, and sleep disordered breathing. Intervention trials are needed to determine whether treatment of insomnia, correction of circadian disruption, and reduction of periodic limb movements produce sustained improvements in blood pressure control. Particular attention should be paid to the influence of age, sex, obesity, and cardiometabolic comorbidities. Such studies may help clarify which sleep related factors have a causal role in hypertension and which primarily reflect associated health conditions.

5. LIMITATIONS

This review has several limitations. First, the included studies were selected by the authors based on their relevance rather than through a strictly predefined systematic protocol, which may introduce selection bias. Second, the literature search was limited to PubMed/MEDLINE and Google Scholar, and therefore some relevant publications indexed in other databases may have been missed. Third, no formal assessment of methodological quality or risk of bias was performed, meaning that the conclusions are based on studies of varying methodological reliability. Fourth, the included studies differed substantially in study design, sample size, and methods used to assess sleep and blood pressure. Both subjective methods, such as questionnaires, and objective methods, including polysomnography, were used, which limits comparability between studies. Fifth, the analyzed populations were heterogeneous in terms of age, sex, ethnicity, place of residence, and comorbidities. These factors may influence both sleep characteristics and blood pressure and may therefore act as confounders. In addition, differences in measurement protocols, follow up duration, and, in some studies, the absence of control groups may have contributed to the inconsistency of the findings.

6. CONCLUSIONS

Sleep disturbances are associated with blood pressure dysregulation through sympathetic activation, impaired nocturnal blood pressure dipping, activation of the hypothalamic-pituitary-adrenal and renin-angiotensin-aldosterone systems, and, in obstructive sleep apnea, recurrent intermittent hypoxia.

The strongest and most consistent evidence concerns obstructive sleep apnea, particularly in patients with resistant or poorly controlled hypertension. Short sleep duration, insomnia accompanied by objectively reduced sleep, and circadian disruption are also associated with hypertension, although the evidence is less consistent. Findings regarding restless legs syndrome and periodic limb movements during sleep remain heterogeneous. Assessment of sleep disorders and sleep patterns may help identify potentially modifiable factors contributing to inadequate blood pressure control.

DISCLOSURE

Author Contributions

Conceptualization: Katarzyna Łysynkiewicz, Jan Szewczyk, Zuzanna Wątek, Patrycja Krawczyk, Maria Bołoz, Sylwia Haba. Methodology: Katarzyna Łysynkiewicz, Jan Szewczyk, Zuzanna Wątek, Patrycja Krawczyk, Maria Bołoz, Sylwia Haba. Literature review and data extraction: Katarzyna Łysynkiewicz, Zuzanna Wątek, Patrycja Krawczyk, Sylwia Haba, Izabela Grzyb. Writing, original draft preparation: Jan Szewczyk, Zuzanna Wątek, Alicja Smolińska, Patrycja Krawczyk, Ewa Dapkiewicz, Dawid Gąsowski, Maria Bołoz. Writing, review and editing: Katarzyna Łysynkiewicz, Izabela Grzyb, Jan Szewczyk, Zuzanna Wątek, Sylwia Haba, Dawid Gąsowski. Supervision: Katarzyna Łysynkiewicz.

All authors reviewed and approved the final version of the manuscript.

Use of Artificial Intelligence

Artificial intelligence tools were used solely for language editing and improvement of grammatical accuracy. All content was critically reviewed by the authors to ensure scientific accuracy and logical consistency. The authors take full responsibility for the final content of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

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