According to a new clinical study published in the New England Journal of Medicine, baxdrostat, a drug developed to treat hypertension, has produced an unexpected scientific finding. Patients who stopped taking the medication continued to have lower blood pressure over the following two years, with some maintaining normal blood pressure levels even without treatment.
More than one billion people worldwide have high blood pressure. In approximately 5–10% of hypertension cases, the cause may be primary aldosteronism — a condition in which the adrenal glands produce excessive amounts of the hormone aldosterone. This can sometimes be caused by a small nodule or benign tumor on the gland. Excess aldosterone causes the kidneys to retain salt, which, in turn, significantly raises blood pressure.
Until now, the standard treatment for this condition has been surgical removal of the affected adrenal gland. However, because other factors often contribute to the development of hypertension, surgery does not always result in a complete cure.
The new drug, baxdrostat, belongs to a class of medications known as aldosterone synthase inhibitors (ASIs) and directly suppresses the production of this hormone. Earlier this year, the drug was approved in the United States for patients whose hypertension does not respond to conventional treatments.
A study led by Morris Brown, a hypertension specialist and professor at Queen Mary University of London, found that after taking the drug daily for 6 to 12 months, patients experienced a substantial reduction in blood pressure. Follow-up examinations conducted two years after treatment had been completely discontinued confirmed that the effect persisted.
“This is a very exciting phenomenon. Almost a quarter of the patients stopped all treatment completely and maintained absolutely normal blood pressure,” Morris Brown notes.
Why does the effect persist after patients stop taking the drug? Scientists have a possible explanation for this phenomenon, based on an experiment conducted in mice nearly 20 years ago.
Brown hypothesizes that when baxdrostat suppresses aldosterone production, the amount of reactive oxygen species (ROS) inside cells increases sharply. According to his hypothesis, these molecules may selectively destroy the cells responsible for producing excessive amounts of aldosterone.
“These oxygen radicals kill the target cells, and they disappear. We think this is the mechanism, and we are now testing the process directly in the laboratory,” Brown explains.
Mason Freeman, a professor of medicine at Harvard University who was involved in the study, emphasizes that if this effect is confirmed in ongoing large-scale clinical trials, the standards for diagnosing and treating the condition could change dramatically.
According to Freeman, if the effect is confirmed in larger studies, patients could potentially be treated with ASI-class drugs as soon as the disease is first suspected. If they respond positively to treatment, they may be able to avoid invasive diagnostic procedures and surgery.
