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Researchers at the University of Virginia School of Medicine's Department of Pharmacology have made a groundbreaking discovery by mapping the brain's primary control center for regulating blood pressure fluctuations. Led by Stephen B.G. Abbott, PhD, the Abbott Lab has pinpointed a specific group of neurons in the brainstem known as rostral ventrolateral medulla C1 (RVLMC1) adrenergic neurons. These cells play a crucial role in maintaining stable blood pressure during everyday transitions like waking from sleep, shifting between sleep stages, or engaging in physical activity.
This finding addresses a long-standing question in neuroscience: how does the body keep blood pressure steady moment-to-moment despite constant changes in behavior and arousal levels? Traditional blood pressure checks focus on average readings, but short-term blood pressure variability (BPV) – the rapid ups and downs – is increasingly recognized as a key risk factor for cardiovascular diseases, strokes, and organ damage. The UVA team's work reveals that even when average blood pressure remains normal, instability in these neural signals can lead to harmful fluctuations.

🧠 Understanding RVLMC1 Neurons: The Brain's Blood Pressure Stabilizers
The brainstem, often called the body's 'control center' for automatic functions like breathing and heart rate, houses the rostral ventrolateral medulla (RVLM). Within this region, RVLMC1 neurons are a subset of adrenergic neurons – cells that release norepinephrine, a neurotransmitter involved in the body's fight-or-flight response. These neurons integrate two vital inputs: sensory feedback from arterial baroreceptors (pressure sensors in blood vessel walls) and central signals related to arousal and behavioral state changes.
To grasp their importance, consider daily life. When you stand up quickly after sitting, blood pressure can drop momentarily due to gravity pooling blood in the legs. The baroreflex – a rapid reflex arc – normally counters this by increasing heart rate and constricting vessels. RVLMC1 neurons fine-tune this process, buffering against overcorrections that cause swings. Without them functioning properly, even normal activities could lead to erratic pressure changes, straining the heart and vessels over time.
The Abbott Lab's research demonstrates that these neurons activate dynamically: they fire rapidly during arousal from non-rapid eye movement (NREM) sleep, maintain steady activity in rapid eye movement (REM) sleep, and ramp up further during movement. This state-dependent pattern ensures blood pressure adapts smoothly, preventing spikes or drops that contribute to fatigue, dizziness, or worse health outcomes.
📊 The Groundbreaking Study: Methods and Key Discoveries
The study, published in Circulation Research on February 13, 2026 (DOI: 10.1161/CIRCRESAHA.125.326792), utilized cutting-edge techniques in freely behaving rats to mimic natural conditions. Researchers employed genetically targeted fiber photometry, a method that uses light to monitor calcium levels as a proxy for neural activity in real-time. This allowed precise tracking of RVLMC1 neuron firing across sleep-wake cycles and voluntary movements.
Key experiments included:
- Sinoaortic denervation to isolate baroreflex contributions, revealing how pressure feedback modulates neuron activity during blood pressure changes or sleep transitions.
- Selective genetic ablation of RVLMC1 neurons using targeted toxins, which left average blood pressure unchanged but caused dramatic instability during arousal and activity – blood pressure swings increased markedly.
"What we found is that a loss of just a few hundred nerve cells leads to unstable blood pressure even though the mean blood pressure was normal," Abbott explained. "This shows that the system that keeps blood pressure steady from moment to moment is no longer working." The team, including George M.P.R. Souza, Harsha Thakkalapally, Faye E. Berry, Leah F. Wisniewski, Ulrich M. Atongazi, and Daniel S. Stornetta, conducted this NIH-funded work (grant HL148004) without financial conflicts.
These results highlight how RVLMC1 neurons act as an integrative hub, blending arousal-driven commands from higher brain areas with peripheral sensory input to dampen variability. For context, short-term BPV is measured over minutes to hours and correlates with risks beyond average hypertension readings, such as endothelial damage and atherosclerosis progression.
💉 Health Implications: From Multiple System Atrophy to Everyday Risks
The discovery has profound implications for conditions involving blood pressure dysregulation. In multiple system atrophy (MSA), a rare neurodegenerative disorder akin to Parkinson's, RVLMC1 neurons degenerate, leading to orthostatic hypotension – dangerous drops in blood pressure upon standing – and supine hypertension. Patients experience fainting, falls, and reduced life expectancy, underscoring the neurons' clinical relevance.
Beyond MSA, unstable BPV appears in aging, diabetes, sleep apnea, and even 'masked hypertension' where clinic readings seem fine but home monitoring reveals volatility. The UVA findings suggest brainstem dysfunction could underlie these, opening avenues for neuron-targeted therapies like neuromodulation or drugs enhancing adrenergic signaling. For instance, precise interventions might stabilize pressure without broad sympathetic blockade, reducing side effects of current antihypertensives.
Public health-wise, with cardiovascular disease claiming 17.9 million lives yearly (per WHO data), targeting BPV could prevent strokes and heart failure. Lifestyle factors like exercise and sleep hygiene indirectly support these neurons, but pharmacological precision beckons for high-risk groups.
For more on university-driven medical breakthroughs, explore higher education news or pharmacology research jobs advancing such discoveries.
🔬 The Abbott Lab: Pioneering Integrative Neurobiology at UVA
The Abbott Lab, housed at UVA's Department of Pharmacology, specializes in how the brain orchestrates cardiorespiratory homeostasis amid behavioral shifts. Using tools like optogenetics, electrophysiology, and RNA sequencing in rodent models, the team dissects neural circuits linking stress, emotion, and autonomic control. Their work builds on prior UVA neuroscience feats, such as identifying blood-loss alarms and pressure-sensing barometers.
Stephen Abbott, with expertise in autonomic neuroscience, leads a collaborative environment fostering PhD students and postdocs. Recent outputs include publications on breathing-cardiovascular crosstalk, positioning the lab at the forefront of hypertension research. UVA's vibrant ecosystem, including the Cardiovascular Research Center, amplifies these efforts.
Aspiring researchers can pursue similar paths through faculty positions, postdoc opportunities, or university jobs in pharmacology and neuroscience. Rate professors like those at UVA via Rate My Professor for insights into top labs.

🌍 Future Directions: Therapeutic Horizons and Broader Impact
Looking ahead, the Abbott Lab aims to translate findings to humans via imaging and biomarkers for RVLMC1 integrity. Potential therapies include:
- Gene therapies restoring neuron function in MSA.
- Designer drugs modulating norepinephrine release selectively.
- Non-invasive brain stimulation to enhance baroreflex gain.
Clinically, wearable BP monitors could track variability, guiding personalized treatments. In higher education, this underscores pharmacology's role in precision medicine, attracting talent to programs like UVA's.
Read the full study for details: UVA Abbott Lab Announcement or Abbott Lab Site.
For career advice in neuroscience, check how to write a winning academic CV.
📝 Wrapping Up: Stabilizing the Future of Blood Pressure Research
The UVA Abbott Lab's mapping of the brain's blood pressure control center illuminates a neural linchpin for health stability. By decoding RVLMC1 neurons' role in taming variability, this work paves the way for smarter hypertension management and neuroprotection. As research progresses, it promises to transform lives affected by hidden pressure instabilities.
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