- Published on
A Third Hidden Driver of High Blood Pressure Has Been Discovered β And a Potential Fix
- Authors
- Name
- DeepHorus
Scientists have identified a potential third driver of high blood pressure, beyond the two well-known mechanisms, and an experimental drug that may target it. The discovery, published in Communications Biology, points to inflammation-resolution pathways as a key player in hypertension. These pathways tell the immune system to stand down after an injury or infection, and their failure may contribute to chronic high blood pressure. Researchers from institutions in Australia and Singapore led the study, which also tested a compound called 17b in mouse models. The findings could open new avenues for treating hypertension and repairing organ damage.
Doctors typically focus on two main drivers of high blood pressure: the sympathetic nervous system, which controls the body's fight-or-flight response, and the renin-angiotensin-aldosterone system, a set of hormones that regulate blood volume and flow. Chronic inflammation has been linked to both systems, but its resolution pathways were not previously considered central to hypertension. The new research shows these pathways may be far more important than earlier thought. The study specifically examined formylpeptide receptors, which act as toggle switches that tell immune cells their job is done.
In experiments on mice with hypertension, compound 17b produced a modest drop in blood pressure. More notably, the drug reduced stiffness in the main aorta artery and decreased dangerous scar tissue build-up, known as fibrosis, in the heart and kidneys. These protective effects occurred alongside only moderate reductions in blood pressure, suggesting the drug's benefits go beyond simply lowering pressure. The researchers say this indicates the compound directly repairs damage caused by chronic inflammation.
The findings matter because existing anti-inflammatory drugs suppress the immune system broadly and can raise blood pressure. Compound 17b works differently by waking up the body's natural inflammation-resolution pathways instead of suppressing immunity. This precision may avoid the side effects of current treatments. The drug had already shown promise in protecting the heart from damage, and this new study extends its potential to hypertension.
βThis study provides an opportunity to advance understanding of neuro-immune interactions in hypertension,β the researchers wrote. They believe FPR agonism is a promising therapeutic strategy for lowering blood pressure and reversing renovascular fibrosis. The approach could complement existing medications or serve as an alternative for patients who cannot tolerate current drugs. However, the team cautions that the experiments were only conducted in mice, and further research is needed to confirm the effects in humans.
The discovery also highlights the importance of inflammation-resolution pathways as a target for future treatments. While compound 17b is not suggested as a direct replacement for current blood pressure medications, it may be used alongside them to help heal inflammation and scarring. The researchers emphasize that more work is needed, but the potential is significant. If successful in human trials, this could lead to a new class of hypertension therapies that address underlying organ damage, not just blood pressure numbers.
