A potential shift from managing hypertension to addressing a cause

A new approach to a common hormone-driven form of high blood pressure may produce benefits that continue after medication is stopped, according to a small study led by Queen Mary University of London.

The treatment is called extended aldosterone synthase inhibition, or EASI. It uses a newer class of medicines intended to suppress production of aldosterone, a hormone that helps regulate salt balance. In some people, excess aldosterone is a key driver of high blood pressure. The researchers report that treating participants for six to 12 months was followed by sustained reductions in excess hormone production and by partial or complete resolution of hypertension for as long as two years after treatment ended.

The findings, published in the New England Journal of Medicine, are early and involve only 14 people. But they raise a consequential possibility: for a defined group of patients, treatment could eventually aim to reverse an underlying hormonal problem rather than simply control its effects indefinitely.

Why aldosterone matters

Hypertension affects millions of people, but it is not a single disease with a single cause. The study focuses on primary aldosteronism, a condition in which benign nodules in the adrenal glands make too much aldosterone. The excess hormone causes the kidneys to retain more salt, which in turn raises blood pressure.

Queen Mary University of London estimates that primary aldosteronism accounts for between 5% and 10% of high-blood-pressure cases. Conventional treatment can control blood pressure, but it does not necessarily remove the source of excess aldosterone. Until now, the report says, a cure has required surgery to remove an entire adrenal gland.

That makes a durable drug-based alternative especially notable. Rather than targeting blood pressure alone, aldosterone synthase inhibitors are designed to target the enzyme involved in aldosterone production. The EASI strategy extends that inhibition over months, based on the idea that sustained suppression could alter the hormone-producing cells themselves.

What the study found

The study followed 14 participants treated at eight centers in the United States. Each received an aldosterone synthase inhibitor for six to 12 months. After treatment stopped, researchers tracked hormone levels and blood pressure.

They found sustained reversal of excess aldosterone production, along with partial or complete resolution of high blood pressure, for up to two years after treatment ended. According to the report, hormone levels and blood-pressure measurements after treatment remained similar to, or lower than, the levels observed while participants were receiving EASI.

That persistence is central to the result. Many hypertension medicines work only while a patient continues taking them. Here, the reported benefit after discontinuation suggests that prolonged suppression may have changed the condition responsible for the excess aldosterone, at least for some participants.

A hypothesis rooted in earlier work

The rationale for the treatment dates to a 2005 mouse experiment, according to the university. In that work, removing the gene responsible for producing aldosterone synthase caused aldosterone-producing cells to disappear. Researchers at Queen Mary then proposed that prolonged pharmacological inhibition might produce a related effect in people.

The new clinical study is not proof that the same mechanism occurred in every participant. Its importance is that it offers evidence consistent with a lasting biological effect after the inhibitor was withdrawn. The findings also point toward a broader model for treating certain endocrine conditions: suppressing a disease-driving pathway long enough to potentially alter the tissue responsible for it.

What needs to happen next

The limited size of the study means its results should not yet be read as a general cure for hypertension. It involved a specific hormonal subtype, a small number of participants and follow-up of up to two years. Larger studies will be needed to establish how durable the effect is, which patients are most likely to benefit and how the treatment compares with existing medical and surgical care.

Even so, the work highlights the value of identifying the cause of a patient’s high blood pressure. If primary aldosteronism is responsible, a treatment tailored to aldosterone production could offer a very different path from routine long-term blood-pressure management.

For now, EASI remains an emerging clinical strategy rather than a replacement for established care. But the study offers a clear signal that a common, treatable hormonal cause of hypertension may be more reversible than previously assumed.

This article is based on reporting by Medical Xpress. Read the original article.

Originally published on medicalxpress.com