The Sympathetic Nervous System and Hypertension: What the Latest Science Reveals About Your Blood Pressure

Hypertension is often called the “silent killer,” yet most people think of it only in terms of salt, weight, or family history. What rarely gets the spotlight is the hidden force orchestrating high blood pressure: the sympathetic nervous system (SNS). This complex network of nerves acts as the body’s fight-or-flight accelerator, controlling heart rate, vascular tone, and kidney function. When it becomes chronically overactive — a phenomenon known as sympathetic overactivity — blood pressure can rise silently, long before conventional measurements detect a problem (Seravalle & Grassi, 2022).

Recent research reveals that this neural overdrive is not just a byproduct of hypertension; it is often the primary driver. Studies using microneurography and norepinephrine spillover measurements show that nerve firing rates are elevated in high-risk individuals even before they meet diagnostic criteria for hypertension (Grassi, 2021; Sakitani, 2026). Factors like sleep disruption, metabolic dysregulation, and chronic stress amplify this hidden activity, creating a self-reinforcing loop that standard medications may only partially interrupt.

Understanding the SNS’s role reshapes how we think about cardiovascular risk. It explains why some patients with “controlled” blood pressure still develop organ damage, including left ventricular hypertrophy, arterial stiffness, and kidney impairment (Grassi & Drager, 2024). This knowledge also opens the door to cutting-edge interventions — from renal denervation to SNS-targeted pharmacology — that promise to address the root neurological mechanisms rather than merely lowering numbers.

In short, the story of high blood pressure is no longer just about the heart or kidneys — it begins in the brain’s autonomic circuits, silently driving risk in millions worldwide.

Clinical pearls

1. The "Early Warning" System

• Scientific Perspective: Sympathetic overactivity (elevated MSNA) often precedes the clinical diagnosis of hypertension. It acts as a primary pathophysiological driver in pre-hypertensive and high-risk genetic phenotypes, rather than a compensatory response to high pressure.

• Your "fight-or-flight" system can be stuck in the "on" position years before a blood pressure cuff shows a high reading. If you have a family history of heart disease, managing stress and sleep now is a proactive strike against high blood pressure later.

2. Beyond the "Pressure" Number

• Scientific Perspective: Chronic adrenergic activation (excess norepinephrine) is independently cardiotoxic and vasculotoxic. It promotes myocardial fibrosis and arterial stiffening through oxidative stress pathways, even if "cuff" blood pressure appears controlled.

• High blood pressure isn't just about the "plumbing" or the pressure in the pipes; it’s about the "corrosive" stress hormones in your blood. Even if your numbers look okay on medication, high stress levels can still wear down your heart and arteries.

3. The Kidney-Brain "Two-Way Street"

• Scientific Perspective: The renal nerves are bidirectional; efferent signals trigger renin release and sodium retention, while afferent signals provide sensory feedback that sustains central sympathetic outflow in the brain.

• Your kidneys and your brain are constantly "talking" to each other. Your brain tells your kidneys to hold onto salt, and your kidneys tell your brain to stay stressed. Procedures like renal denervation work by "cutting the phone line" to stop this cycle.

4. Sleep Apnea as a Sympathetic "Gas Pedal"

• Scientific Perspective: Nocturnal intermittent hypoxia triggers chemoreceptor-mediated sympathetic bursts that "carry over" into daytime hours, leading to tonically elevated sympathetic tone and resistant hypertension.

• If you stop breathing at night (apnea), your body panics and floods your system with adrenaline to wake you up. This adrenaline doesn't just disappear when you wake up; it stays in your system all day, keeping your blood pressure high even while you’re awake.

5. The Baroreflex "Brake" Failure

• Scientific Perspective: Chronic hypertension leads to "resetting" and impairment of the arterial baroreceptors. This results in the loss of the natural inhibitory "brake" on sympathetic outflow, allowing blood pressure to fluctuate wildly and stay elevated.

• Your body has a built-in "thermostat" that is supposed to lower your heart rate when your blood pressure gets too high. In long-term hypertension, that thermostat breaks, and your body forgets how to naturally "cool down" your blood pressure.

6. The Precision Medicine Shift

• Scientific Perspective: Hypertension is moving toward "phenotyping." New biomarkers (like Neuropeptide Y) and imaging (PET scans) allow for identifying patients with "neurogenic hypertension" who will respond better to SNS-targeted drugs or devices than standard diuretics.

• We are moving away from a "one-size-fits-all" pill for blood pressure. In the near future, doctors will use specific tests to see if your high blood pressure is coming from your brain, your kidneys, or your lifestyle, and pick a treatment that fits your specific "profile."

1. Why the Sympathetic Nervous System Matters in Hypertension

To understand the research, it helps to understand the mechanism. The sympathetic nervous system acts through a network of nerve fibers that innervate the heart, blood vessels, and kidneys. When activated, it releases norepinephrine (noradrenaline), which causes the heart to beat faster and harder, peripheral blood vessels to constrict, and the kidneys to retain sodium and water — all of which raise blood pressure.

Under normal circumstances, this activation is brief and purposeful: it helps you respond to stress, physical exertion, or danger. The problem arises when the system becomes chronically overactive — essentially stuck in "high alert" — elevating blood pressure continuously even at rest.

Measuring this overactivity is technically challenging. The gold standard remains microneurography, a technique that directly records sympathetic nerve firing in peripheral nerves, alongside norepinephrine spillover measurements that estimate how much of the neurotransmitter is being released into the bloodstream from specific organs.

2. New Evidences: Seravalle & Grassi (2022)

Key Takeaway: Sympathetic overactivity is not a byproduct of hypertension — it is a foundational cause, and its markers are measurable long before blood pressure becomes clinically elevated.

Seravalle and Grassi's 2022 review in Autonomic Neuroscience: Basic and Clinical synthesized emerging evidence confirming that sympathetic neural drive is tonically elevated across multiple hypertensive populations. Using microneurographic data, the authors demonstrated that muscle sympathetic nerve activity (MSNA) — the electrical impulse rate measured directly in peripheral nerves — is significantly higher in hypertensive patients than in normotensive controls, even when matched for age and body weight.

Critically, the review highlighted new evidence showing that SNS overactivity precedes frank hypertension in high-risk individuals, including those with prehypertension and a strong family history of cardiovascular disease. This temporal relationship has profound implications: it positions the sympathetic nervous system as a primary pathophysiological player, not merely a secondary responder to elevated pressure.

Seravalle and Grassi also underscored the role of central nervous system sensitization — particularly in the hypothalamus and brainstem — in perpetuating this overactivity. Environmental stressors, sleep disruption, and metabolic dysregulation all amplify central sympathetic outflow, creating a self-reinforcing cycle that standard antihypertensive medications often fail to fully interrupt (Seravalle & Grassi, 2022).

3. A 2026 Mechanistic Frontier: Sakitani's Insights

Key Takeaway: Emerging molecular and neural circuit research is identifying specific sympathetic pathways as druggable targets, pointing toward a new generation of precision antihypertensives.

The most recent addition to this body of literature, Sakitani's 2026 paper in Hypertension Research, takes a granular look at the mechanistic architecture of sympathetic contributions to hypertension. Where earlier reviews characterized the phenomenon broadly, Sakitani maps specific neural circuits — from rostral ventrolateral medulla (RVLM) activity to carotid body chemoreceptor signaling — that are dysregulated in hypertensive states.

One of the paper's most significant contributions is its examination of the carotid body's role as an amplifier of sympathetic tone. In hypertensive individuals, the carotid body becomes hypersensitized to arterial oxygen levels and metabolic signals, triggering disproportionate sympathetic responses. This mechanism, Sakitani argues, may explain why sympathetic overactivity persists even in patients whose blood pressure is partially controlled by medication.

Sakitani also discusses the gut-brain axis as an emerging modulator of sympathetic activity, noting that dysbiosis — disruption of the gut microbiome — may alter neurotransmitter precursor availability and vagal signaling in ways that tip the autonomic balance toward sympathetic dominance. These insights open entirely new therapeutic avenues, from selective carotid body modulation to microbiome-targeted interventions (Sakitani, 2026).

4. A Long Journey Mapped: Grassi's 2021 Roadmap Update

Key Takeaway: Decades of research have established that sympathetic overactivity is universal across hypertensive subtypes, and understanding its triggers is the key to unlocking better treatments.

Grassi's 2021 roadmap in the American Journal of Hypertension is an essential reference that traces the evolution of our understanding from the earliest observations of elevated catecholamines in hypertensive patients through to modern neuroimaging and microneurographic techniques.

A central argument of this paper is that sympathetic overactivity is not a monolithic phenomenon — its pattern, source organ, and intensity vary substantially across hypertensive subtypes. In essential hypertension, overactivity is primarily driven by elevated cardiac and renal sympathetic nerve traffic. In obesity-related hypertension, there is disproportionate activation of renal and skeletal muscle sympathetic pathways, heavily influenced by leptin signaling. In resistant hypertension — where blood pressure remains uncontrolled despite three or more medications — global sympathetic activation is most severe.

Grassi's roadmap also crystallizes the role of baroreflex dysfunction: in healthy individuals, arterial baroreceptors act as a buffering system that dampens sympathetic outflow when blood pressure rises. In hypertension, this feedback loop is progressively impaired, removing a critical brake on sympathetic activity and allowing pressure to spiral further. This insight is not new, but Grassi's synthesis reveals just how central baroreflex failure is across the full hypertension spectrum (Grassi, 2021).

5. The Path to Renal Denervation: Esler, Osborn & Schlaich (2024)

Key Takeaway: The renal sympathetic nerves are a pivotal effector of hypertension, and catheter-based renal denervation — once controversial — is now supported by robust sham-controlled trial evidence as a viable treatment option.

Perhaps no paper in this collection has more immediate clinical relevance than Esler, Osborn, and Schlaich's 2024 review in Hypertension. The authors chart the origins of the sympathetic pathophysiology concept and trace the scientific and clinical journey that led to renal denervation (RDN) as a therapeutic strategy.

The kidneys sit at a critical nexus of sympathetic activity. Efferent sympathetic nerves to the kidney drive renin release, sodium reabsorption, and reduced renal blood flow — all of which push blood pressure upward. Afferent renal sensory nerves simultaneously feed signals back to the brain that sustain central sympathetic outflow. Disrupting this bidirectional communication is the theoretical basis for RDN.

Following the early promise of uncontrolled trials and the sobering results of the initially sham-controlled SYMPLICITY HTN-3 trial, the field recalibrated. Subsequent rigorously designed sham-controlled trials — including SPYRAL HTN-OFF MED and SPYRAL HTN-ON MED — demonstrated significant and durable blood pressure reductions attributable to RDN independent of medication effects.

Esler and colleagues argue compellingly that RDN should no longer be viewed as experimental, but as a legitimate adjunctive intervention for patients with resistant hypertension or those intolerant of multiple antihypertensive medications. The authors also note that proper patient selection — identifying those with the highest degree of renal sympathetic overactivity — will be essential to optimizing outcomes as the procedure enters broader clinical use (Esler et al., 2024).

6. The State of the Art: Grassi & Drager (2024)

Key Takeaway: Sympathetic overactivity is not just a blood pressure problem — it is a systemic cardiovascular risk amplifier that accelerates organ damage independently of the blood pressure elevation itself.

Grassi and Drager's 2024 review in Current Medical Research and Opinion broadens the frame considerably. Rather than examining the SNS purely through the lens of blood pressure elevation, the authors explore how sustained sympathetic overactivity contributes to end-organ damage — including left ventricular hypertrophy, arterial stiffness, renal impairment, and increased arrhythmia risk — through mechanisms that operate partly independently of blood pressure.

The paper synthesizes evidence that excess norepinephrine exerts direct cardiotoxic and vasculotoxic effects: promoting myocardial fibrosis, inducing oxidative stress in arterial walls, and accelerating atherosclerotic plaque development. This means that two patients with identical blood pressure readings can carry dramatically different cardiovascular risks depending on their degree of underlying sympathetic activation.

Grassi and Drager also address the obstructive sleep apnea (OSA)-hypertension nexus, a particularly important intersection. Nocturnal hypoxia triggers intense sympathetic bursts that persist into daytime waking hours, creating a pattern of chronically elevated SNS tone even in patients whose daytime blood pressure appears controlled. Treating OSA, the authors argue, should be considered an essential component of comprehensive hypertension management — not merely a comorbidity to note (Grassi & Drager, 2024).

7. Recent Insights: Grassi et al. (2023)

Key Takeaway: New imaging techniques, biomarkers of sympathetic activation, and pharmacological strategies are converging to make individualized, SNS-targeted hypertension treatment clinically feasible.

The most recently published of the review papers in this collection, Grassi, Dell'Oro, Quarti-Trevano, Vanoli, and Oparil's 2023 paper in Current Hypertension Reports, focuses on what the authors describe as a "translational leap" — the movement from mechanistic understanding to individualized, precision treatment.

Among the key advances highlighted are novel biomarkers of sympathetic activation, including heart rate variability indices, plasma neuropeptide Y levels, and positron emission tomography (PET)-based imaging of cardiac sympathetic innervation, which together allow clinicians to non-invasively characterize a patient's neuroadrenergic profile before selecting treatment.

The paper also reviews the evolving pharmacological landscape. While traditional agents such as beta-blockers and centrally acting antihypertensives like moxonidine remain in use, the authors discuss the promise of selective imidazoline receptor agonists, novel alpha-2 adrenoreceptor modulators, and the potential repurposing of medications like empagliflozin — primarily known as a diabetes drug — that appear to reduce sympathetic outflow as part of their mechanism of action.

Perhaps most importantly, Grassi and colleagues emphasize that no single biomarker or treatment strategy fits all hypertensive patients. The future of SNS-targeted therapy lies in phenotyping — matching the right measurement tools, the right risk stratification, and the right intervention to each individual patient (Grassi et al., 2023).

Connecting the Dots: What These Six Studies Tell Us Collectively

1. Hypertension is More Than Numbers

   • While elevated blood pressure readings are clinically significant, they often mask underlying neurogenic mechanisms.

   • The sympathetic nervous system (SNS) is increasingly recognized as a primary orchestrator of sustained hypertension, not just a secondary response (Seravalle & Grassi, 2022).

   • Understanding these mechanisms shifts the focus from symptom control to addressing root causes.

2. Sympathetic Overactivity: Mechanisms and Consequences

   • Chronic SNS overactivity drives increased heart rate, vascular constriction, and renal sodium retention, silently escalating cardiovascular risk.

   • Microneurography and norepinephrine spillover studies reveal elevated sympathetic nerve firing in hypertensive and pre-hypertensive individuals (Grassi, 2021).

   • Sustained SNS activation contributes to end-organ damage, including left ventricular hypertrophy, arterial stiffness, renal impairment, and accelerated atherosclerosis (Grassi & Drager, 2024).

3. Phenotypic Variability Across Hypertension Subtypes

   • Essential hypertension, obesity-related hypertension, and resistant hypertension display distinct patterns of sympathetic activation.

   • Baroreflex dysfunction removes critical feedback inhibition, perpetuating neurogenic hypertension.

   • Recognition of these phenotypes allows for precision treatment strategies rather than one-size-fits-all therapy.

4. Emerging Mechanistic Insights

   • Recent research maps specific neural circuits contributing to SNS overactivity, including the rostral ventrolateral medulla, carotid body chemoreceptors, and the gut-brain axis (Sakitani, 2026).

   • Dysbiosis, metabolic disruption, and environmental stressors amplify central sympathetic outflow, highlighting non-traditional therapeutic targets

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5. Therapeutic Frontiers: Renal Denervation and Pharmacology

   • Renal denervation (RDN), once controversial, now demonstrates significant, durable blood pressure reduction in sham-controlled trials (Esler et al., 2024).

   • Pharmacologic innovations targeting SNS include selective imidazoline receptor agonists, alpha-2 adrenoreceptor modulators, and repurposed SGLT2 inhibitors with sympatholytic effects.

   • Combining targeted therapies with lifestyle interventions addresses both neurological and cardiovascular contributors to hypertension.

6. Lifestyle and Non-Pharmacologic Interventions

   • Regular aerobic exercise, weight reduction, stress management, and treatment of obstructive sleep apnea (OSA) meaningfully reduce sympathetic tone.

   • Lifestyle modifications complement pharmacological and procedural interventions, providing a holistic approach to SNS-driven hypertension.

7. Precision Medicine and Future Directions

   • Novel biomarkers of sympathetic activity — including heart rate variability indices, plasma neuropeptide Y, and PET imaging — enable individualized risk stratification and therapy selection (Grassi et al., 2023).

   • Future research aims to integrate circuit-level neuroscience with clinical practice, offering personalized neurogenic hypertension management.

   • Understanding the SNS as a central driver allows clinicians to prevent organ damage even before blood pressure elevation becomes clinically apparent.

8. Clinical and Public Health Implications

   • Treating hypertension solely as a hemodynamic disorder risks underestimating cardiovascular risk in patients with persistent sympathetic overactivity.

   • Incorporating sympathetic profiling into routine evaluation could redefine standard hypertension care and improve long-term cardiovascular outcomes.

   • This approach also emphasizes early intervention in high-risk populations, shifting care from reactive to proactive.

9. Conclusion

   • Hypertension is a neurocardiovascular disease as much as it is a vascular condition.

   • The sympathetic nervous system, once considered a background player, is now central to understanding, preventing, and treating high blood pressure.

   • Clinicians, researchers, and patients must recognize that addressing SNS overactivity is key to improving both blood pressure control and cardiovascular health.

Specific lifestyle habits that clinically down-regulate sympathetic tone

1. Respiratory & Vagal Training

The lungs are a direct "remote control" for the nervous system. Slowing your breath physically forces the brain to dampen its "fight-or-flight" signals.

• Resonant Frequency Breathing: Aim for exactly 6 breaths per minute (5 seconds in, 5 seconds out). This creates "coherence" between your heart rate and your breathing, maximizing the baroreflex (your body's internal blood pressure brake).

• Exhalation Focus: Making your exhale longer than your inhale (e.g., 4 seconds in, 8 seconds out) stimulates the vagus nerve, which sends a "safety" signal to the brainstem to lower heart rate.

2. Neurological Exercise Protocols

Not all exercise is equal for the nervous system. Specific types of movement target the sympathetic neural drive differently.

• Zone 2 Aerobic Training: This is low-intensity, steady-state exercise (like a brisk walk where you can still speak in full sentences). Science shows this specifically reduces Muscle Sympathetic Nerve Activity (MSNA), the electrical firing rate of your nerves.

• Isometric Handgrip Training: Holding a sustained, low-level contraction (e.g., squeezing a grip trainer at 30% effort for 2 minutes) triggers a neurological reflex that has been shown in recent trials to lower systemic blood pressure by "resetting" the sympathetic response.

3. Sleep & Circadian Management

Sleep is when the sympathetic nervous system is supposed to "power down." If sleep is disrupted, the SNS stays on "high alert" 24/7.

• Address Sleep Apnea (OSA): If you snore or stop breathing, your brain triggers a massive adrenaline surge to wake you up. Using a CPAP or oral appliance stops these nocturnal "emergency" bursts.

• Temperature Regulation: Keeping your bedroom cool (around 18°C) supports the natural drop in core body temperature required to transition from sympathetic (active) to parasympathetic (restorative) dominance.

4. Metabolic & Dietary Signals

The brain monitors your blood chemistry to determine if it should trigger a stress response.

• Potassium-to-Sodium Ratio: High potassium levels (from leafy greens and beans) help the kidneys signal the brain to "calm down" the sympathetic outflow. It isn't just about less salt; it's about more potassium.

• Gut-Brain Axis Care: Emerging 2026 research (Sakitani) suggests that a diverse, high-fiber diet reduces inflammation that can "irritate" the nerves connecting the gut to the brain, which otherwise keeps the SNS overactive.

5. Biofeedback & Mindfulness

These techniques help you "see" your nervous system in real-time so you can learn to control it.

• HRV Monitoring: Using a wearable device to track Heart Rate Variability (HRV). A high HRV generally indicates a relaxed sympathetic system. By watching these numbers, you can identify which specific stressors (work, caffeine, etc.) are "spiking" your system.

• Meditation for Brainstem Cooling: Regular mindfulness practice has been shown to physically change the "excitability" of the Rostral Ventrolateral Medulla (RVLM)—the area of the brain that acts as the master switch for blood pressure.

Frequently Asked Questions (FAQs)

1. What is sympathetic nervous system overactivity, and how is it detected? Sympathetic nervous system overactivity refers to a state of chronically elevated neural signaling through the SNS, causing persistent increases in heart rate, vascular resistance, and renal sodium retention. The gold standard for detecting it is microneurography — directly recording sympathetic nerve firing in peripheral nerves — though clinicians can also use norepinephrine spillover measurements, heart rate variability analysis, and emerging biomarkers like neuropeptide Y.

2. Does everyone with hypertension have sympathetic overactivity? Not necessarily. Sympathetic overactivity is most consistently demonstrated in essential hypertension, obesity-related hypertension, and resistant hypertension. Its degree varies significantly across individuals, which is why personalized assessment of sympathetic tone is an important frontier in hypertension management (Grassi, 2021; Grassi et al., 2023).

3. Can treating the sympathetic nervous system cure hypertension? Current evidence suggests that SNS-targeted treatments — including renal denervation and pharmacological agents — can produce meaningful and sustained reductions in blood pressure, particularly in resistant cases. However, hypertension is multifactorial, and SNS treatment is generally considered an important component of a comprehensive management strategy rather than a standalone cure (Esler et al., 2024).

4. What is renal denervation, and is it safe? Renal denervation is a minimally invasive catheter-based procedure that uses radiofrequency or ultrasound energy to ablate the sympathetic nerve fibers running along the renal arteries. It has been shown to reduce blood pressure independently of medication in recent sham-controlled trials. Its safety profile is considered acceptable, with the main risks relating to the catheterization procedure itself (Esler et al., 2024).

5. How does sleep apnea connect to sympathetic overactivity and hypertension? Obstructive sleep apnea causes repeated episodes of nocturnal hypoxia, each of which triggers an intense sympathetic surge. Over time, this chronic intermittent activation sensitizes the SNS and elevates daytime sympathetic tone, contributing to hypertension that can be difficult to treat without also addressing the underlying sleep disorder (Grassi & Drager, 2024).

6. Are there new drugs targeting the sympathetic nervous system for hypertension? Yes, several are under investigation or in early clinical use. These include selective imidazoline receptor agonists, novel alpha-2 adrenoreceptor modulators, and SGLT2 inhibitors (like empagliflozin), which appear to reduce sympathetic outflow as part of their broader cardiovascular benefit. Carotid body modulation is also being explored as a target, particularly in patients with chemoreflex-driven sympathetic overactivity (Sakitani, 2026; Grassi et al., 2023).

7. Can lifestyle changes reduce sympathetic overactivity? Yes. Regular aerobic exercise is one of the most well-established non-pharmacological interventions for reducing resting sympathetic nerve activity. Weight loss in obese individuals reduces leptin-driven sympathetic activation. Stress reduction techniques and treatment of sleep apnea also meaningfully lower sympathetic tone. These interventions are complementary to, not replacements for, pharmacological management in most clinical cases.

Author’s Note:

Hypertension is often discussed in terms of numbers on a blood pressure cuff, but emerging research reveals a more nuanced story — one in which the sympathetic nervous system (SNS) plays a central, and often overlooked, role. This article synthesizes the latest scientific insights from 2021–2026 to provide clinicians, researchers, and informed readers with a comprehensive understanding of sympathetic overactivity, its mechanisms, and its impact on cardiovascular health.

Our goal is to bridge the gap between complex neurophysiological research and practical clinical implications. By highlighting advances in renal denervation, pharmacological targeting, and lifestyle interventions, we hope to empower readers to appreciate that managing blood pressure is not just about lowering numbers but also about addressing the neurological drivers behind the disease.

While this post draws on high-level scientific literature, it is intended for educational purposes only and does not replace personalized medical advice. Individuals with hypertension or related cardiovascular conditions should consult qualified healthcare professionals before making any changes to their treatment plans.

Disclaimer: This article is for informational purposes only and does not constitute medical advice. Individual circumstances vary, and treatment decisions should always be made in consultation with qualified healthcare professionals.

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References

Esler, M. D., Osborn, J. W., & Schlaich, M. P. (2024). Sympathetic pathophysiology in hypertension origins: The path to renal denervation. Hypertension, 81(6), 1194–1205. https://doi.org/10.1161/HYPERTENSIONAHA.123.21715

Grassi, G. (2021). The sympathetic nervous system in hypertension: Roadmap update of a long journey. American Journal of Hypertension, 34(12), 1247–1254. https://doi.org/10.1093/ajh/hpab124

Grassi, G., & Drager, L. F. (2024). Sympathetic overactivity, hypertension and cardiovascular disease: State of the art. Current Medical Research and Opinion, 40(sup1), 5–13. https://doi.org/10.1080/03007995.2024.2305248

Grassi, G., Dell'Oro, R., Quarti-Trevano, F., Vanoli, J., & Oparil, S. (2023). Sympathetic neural mechanisms in hypertension: Recent insights. Current Hypertension Reports, 25(10), 263–270. https://doi.org/10.1007/s11906-023-01254-4

Sakitani, N. (2026). The sympathetic nervous system in the pathophysiology of hypertension: Mechanistic insights and therapeutic implications. Hypertension Research. https://doi.org/10.1038/s41440-026-02589-6

Seravalle, G., & Grassi, G. (2022). Sympathetic nervous system and hypertension: New evidences. Autonomic Neuroscience: Basic and Clinical, 238, 102954. https://doi.org/10.1016/j.autneu.2022.102954