By Clinical Research News Staff 

March 17, 2026 | Hypertension, also known as high blood pressure, has long been thought of as primarily a disorder of the heart, kidneys, or blood vessels. A growing body of evidence suggests that, in a substantial proportion of patients, the condition originates in the brain. 

Julian Paton, Ph.D., professor of translational physiology at the University of Auckland (New Zealand) co-led a recent rat study that centered on neurogenic hypertension, a subtype estimated to account for up to 60% of essential hypertension cases (Circulation Research, DOI: 10.1161/CIRCRESAHA.125.32667). In these patients, persistently elevated sympathetic nervous system activity—the “fight-or-flight” response—drives blood pressure upward, contributes to inflammation, and accelerates end-organ damage. Standard antihypertensive drugs can lower blood pressure numbers, but they do little to suppress this underlying sympathetic overactivity. 

Paton’s team identified a critical neural hub: the lateral parafacial region of the brain stem. This region was shown to be tightly coupled to sympathetic nerve outflow. When the researchers selectively silenced these neurons in hypertensive animals, sympathetic activity fell and blood pressure normalized. The findings suggest that abnormal breathing-related neural signals can directly sustain hypertension. 

Crucially, this translational relevance lies not in targeting the brain directly, but in identifying what drives these neurons in disease. The team found that hyperactivity in the carotid bodies—tiny oxygen-sensing organs located in the neck—acts as the upstream trigger. In hypertension, the carotid bodies appear to generate excessive adenosine triphosphate (ATP) signaling, overstimulating the brain stem and, in turn, the sympathetic nervous system. 

This insight has paved the way for a first-in-human clinical trial using a repurposed drug: gefapixant (marketed as Lyfnua), a Merck-owned purinergic receptor antagonist that is already approved in parts of Europe and Asia for chronic cough. By blocking ATP signaling at the carotid bodies, researchers hope to dampen sympathetic drive and lower blood pressure without penetrating the brain or disrupting normal respiratory control. The planned trial will be small, enrolling around 20 patients, but methodologically intensive.  

In parallel, Paton’s group is testing a precision-medicine approach to hypertension management. Using a DNA swab and an algorithm that integrates variants across 17 blood pressure–related genes, the researchers aim to predict which drug or drug combination is most likely to work for an individual patient from the outset. The goal is to replace today’s trial-and-error prescribing with a more rational, data-driven strategy. 

To read the full story written by Deborah Borfitz, visit Diagnostics World News.