A groundbreaking new study has found compelling evidence that a specific brain region could be directly contributing to some cases of high blood pressure. Even more importantly, the researchers believe they have found a way to reverse it.
According to the study, carried out by a collaborative team from the University of São Paulo in Brazil and the University of Auckland in New Zealand, the lateral parafacial (pFL) brain region can trigger biological changes that drastically raise blood pressure. This revelation could eventually change the way we treat the world’s most common cardiovascular condition.
The Breathing and Blood Pressure Connection
The pFL region of the brain is primarily linked to breathing control—specifically managing forceful and deliberate exhalations, such as what happens when we exercise, cough, or laugh.
However, in tests carried out on rats, researchers discovered that it can also do something else: actively tighten up blood vessels. That unique combination of breath control and blood vessel signaling could be driving hypertension in many cases.
This study suggests that pFL neurons link changes in our breathing rhythms—which wouldn’t necessarily be noticeable to the individual—to increased activity in the sympathetic nervous system (our body’s ‘fight-or-flight’ response).
Why Do Traditional Medications Fail?
Currently, it is estimated that around 40 percent of people with high blood pressure still have uncontrolled levels despite taking standard anti-hypertensive medications.
“Given that around 50 percent of patients with hypertension have a neurogenic component, the challenge is to understand mechanisms generating sympatho-excitation in hypertension,” the researchers wrote in their published paper in the journal Circulation Research. “Such a revelation would provide much-needed clinical orientation for new therapeutic strategies.”
The Link to Sleep Apnea
The findings also go a long way in explaining why individuals who suffer from sleep apnea—a condition characterized by breathing interruptions during the night—have a significantly higher risk of high blood pressure.
While pFL neurons aren’t actively involved in normal resting breathing, they rapidly fire up in response to high CO2 or low oxygen levels—which is exactly what happens during an apnea episode.
A New Pathway for Treatment
In their experiments, researchers used genetic engineering techniques to turn pFL neurons on or off in rats, while monitoring breathing-related nerve activity, sympathetic nerve activity, and blood pressure.
- Activating the Neurons: When researchers activated pFL neurons, it triggered other brain circuits that ultimately raised the animals’ blood pressure and constricted blood vessels.
- Inactivating the Neurons: “We discovered that, in conditions of high blood pressure, the lateral parafacial region is activated and, when our team inactivated this region, blood pressure fell to normal levels,” explained physiologist Julian Paton from the University of Auckland.
Targeting the Carotid Bodies
While these findings are currently limited to animal models, the urgent need for new human treatment options remains. The next challenge is figuring out how drugs might be able to target the pFL neurons without interfering with other brain functions.
The research team is looking at carotid bodies—clusters of cells that act like tiny sensors in the neck. Because these sensors influence pFL neurons from outside the brain, targeting them might be enough to keep the pFL region in check.
“Our goal is to target the carotid bodies, and we are importing a new drug that is being repurposed by us to quench carotid body activity and inactivate remotely the lateral parafacial region safely, i.e., without needing to use a drug that penetrates the brain,” Paton stated.
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