Redefining Hypertension Treatment with Brain’s Control Circuit

By Bio-IT World Staff 

February 11, 2026 | For decades, the industry’s approach to treating high blood pressure has centered on various organs—the heart, kidneys, and blood vessels. A new study suggests that this strategy may address downstream effects rather than the root cause. According to Julian Paton, Ph.D., professor of translational physiology at the University of Auckland, the primary driver of hypertension in a majority of patients may reside in the brain. 

The study, published in Circulation Research (DOI: 10.1161/CIRCRESAHA.125.32667) identifies a previously underappreciated neural circuit linking respiration and sympathetic nervous system activity. Specifically, neurons in the lateral parafacial region of the brain stem appear to directly amplify sympathetic nerve firing, a major contributor to sustained high blood pressure. In hypertensive rat models, silencing this region normalized blood pressure by reducing chronic sympathetic overactivity, a hallmark of neurogenic hypertension. 

The implications are substantial. Rather than layering drugs that indirectly lower blood pressure, Paton’s team is pursuing interventions that target the causal neurobiological mechanism itself. Central to this strategy is drug repurposing. The researchers plan to test gefapixant (Lyfnua), a Merck-owned purinergic receptor antagonist already approved in parts of Europe and Asia for chronic cough. Gefapixant blocks ATP-mediated signaling, which the team has identified as the biochemical trigger that overstimulates the carotid bodies—small sensory organs in the neck that feed excitatory signals into the brainstem circuit driving hypertension. 

This peripheral entry point is a critical translational advantage. While optogenetics and viral vectors were used in animal studies to manipulate brain stem neurons, the clinical strategy avoids direct brain intervention. Instead, by dampening pathological signaling at the carotid bodies, researchers aim to indirectly suppress the overactive neural circuit without requiring drugs that cross the blood–brain barrier. This approach reduces safety risks and accelerates development timelines. 

Paton’s team is also developing a novel algorithm that integrates data from a DNA swab test, analyzing variants across 17 blood-pressure-related genes. The goal is to predict which drug or drug combination will work best for an individual patient from the outset, reducing today’s trial-and-error prescribing practices. This pharmacogenomic approach aligns with broader trends toward personalized medicine and data-driven treatment selection. 

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