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Researchers have identified a brainstem pathway that can raise blood pressure in rats by linking forceful expiration to the sympathetic nerves that tighten blood vessels. Turning down activity in that pathway lowered pressure in hypertensive rats. The finding suggests a possible contributor to some cases of high blood pressure—not a confirmed cause in people—and the proposed treatment remains experimental.
What did the researchers find?
In a study published online on 17 December 2025 and in Circulation Research on 16 January 2026, Karolyne S. Magalhães and colleagues investigated neurons in the brainstem’s lateral parafacial region, or pFL. They studied normotensive and hypertensive rats, using viral, optogenetic and pharmacogenetic methods to activate or inhibit pFL neurons while measuring respiratory motor output, sympathetic activity and arterial pressure. The study’s PubMed abstract describes the methods and findings.
When the team activated pFL neurons, the rats produced active expiration—forceful breathing out—and sympathetic activity increased during expiration. Blood pressure rose. The researchers also found pFL projections to presympathetic neurons in the rostral ventrolateral medulla (RVLM) and A5 region, and stronger pFL-to-RVLM transmission in hypertensive rats.
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Repair Windows errors before they cause bigger problemsFix Now →Fix the driver behind crashes, sound loss and screen glitchesFind Drivers →In the hypertensive rat model, inactivating the pFL lowered blood pressure to normal levels, according to the University of Auckland’s account of the work. Lead researcher Julian Paton said: “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.” That is a report of an animal experiment, not evidence that disabling this region would safely or effectively treat people.
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How could breathing and blood pressure be connected?
The pFL is associated with active expiration: the more forceful exhalations used in actions such as coughing, laughing or exercising. The study suggests that activity in this brainstem region can also influence sympathetic pathways that help regulate blood-vessel constriction. In the rats, activating the pathway linked active expiration with increased sympathetic activity and higher pressure.
This does not show that ordinary breathing causes hypertension, or that people can control high blood pressure by changing how they breathe. It identifies a neural circuit for further study in rats; whether it has the same role in human hypertension has not been established.
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Is there a treatment based on this finding?
Not yet. The researchers have proposed targeting the carotid bodies, small clusters near the carotid arteries that sense oxygen levels, to influence pFL activity indirectly. The aim would be to avoid a drug that has to enter the brain. Paton told the University of Auckland that the team was importing a drug for research to “quench carotid body activity” and inactivate the pFL remotely. This is a research plan, not a validated medicine or treatment available to patients.
The university says the approach could be relevant to people with sleep apnoea, because breathing pauses at night can activate the carotid bodies. That possibility still requires testing; the study does not establish that this approach treats sleep apnoea or high blood pressure in people.
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How does this differ from the separate carotid-body study?
A separate 2025 University of Auckland report described rat-model research in which the carotid body responded to high blood pressure by activating the sympathetic nervous system. That is related to the proposed carotid-body approach, but it is not the same experiment as the pFL study. The university says researchers still need to confirm whether humans respond in the same way.
What does the study’s “40%” figure mean?
The study abstract states that 40% of treated patients remain hypertensive. This is background context about treated patients, not a result measured in the rat experiments and not an estimate of how many cases involve pFL activity.
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What should people with high blood pressure do?
This animal study does not justify changing medication, seeking an experimental drug or replacing established care. Anyone concerned about blood pressure should discuss measurement and treatment with a qualified healthcare professional. The potential pFL pathway is an early research finding, not a clinical recommendation.
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