A Year of Pills May Cure a Common Hormonal Cause of High Blood Pressure

Millions of people take daily medication to manage high blood pressure, accepting it as a lifelong requirement. Now, a small but striking study suggests that for one common hormonal form of the condition, a finite course of pills might offer a lasting cure.[1][4]

Researchers at Queen Mary University of London have found that a 6-to-12-month treatment with a new class of drugs can put primary aldosteronism into remission. The benefits persisted long after the patients stopped taking the medication.[2][4]

The findings, published in the New England Journal of Medicine, challenge the assumption that hypertension always requires permanent pharmacological management. For a subset of patients, the underlying cause of their elevated blood pressure appears to have been reversed.[1][4]

"It’s very exciting to see," said Professor Morris Brown, a hypertension specialist at Queen Mary University of London who led the research. "Just under a quarter of the patients came off all treatment and had completely normal blood pressure."[1]

The study followed 14 people treated at eight different medical centers across the United States. While the cohort is small, the durability of the results has prompted researchers to launch a larger prospective trial to confirm the curative potential.[4]

The hormonal driver of hypertension

Primary aldosteronism is responsible for an estimated 5 to 10 percent of all hypertension cases worldwide. The condition occurs when benign nodules in the adrenal glands produce excessive amounts of the hormone aldosterone.[1][4]

Aldosterone normally helps the body regulate its balance of sodium and potassium. When the adrenal glands generate too much of it, the kidneys are signaled to retain excess salt, which in turn holds onto water and drives blood pressure up.[1][2]

Patients with this specific hormonal imbalance often struggle to control their blood pressure using standard antihypertensive medications. Their condition leaves them at a significantly elevated risk for heart attacks, strokes, and kidney failure compared to those with essential hypertension.[1][3]

Until now, the only way to achieve a lasting cure for primary aldosteronism was through a surgical intervention. Doctors would have to surgically remove the entire affected adrenal gland to stop the excessive hormone production at its source.[1][4]

Surgery is highly effective, but it requires a hospital stay, carries surgical risks, and results in the permanent loss of an adrenal gland. Furthermore, if other factors contribute to a patient's high blood pressure, the operation might not provide a complete cure.[1]

Blocking the responsible enzyme

The new approach relies on a treatment strategy known as extended aldosterone synthase inhibition, or EASI. Patients in the study took a drug called baxdrostat, which is designed to block the specific enzyme required to manufacture aldosterone.[1][4]

Baxdrostat suppresses the blood pressure-raising hormone directly at its source in the adrenal glands. By taking the medication daily for a period of 6 to 12 months, the researchers aimed to shut down the overactive cells completely.[1][2]

The scientific logic behind this prolonged blockade dates back to a pivotal 2005 experiment conducted in mice. In that study, researchers found that deleting the gene responsible for producing aldosterone synthase actually caused the aldosterone-making cells to disappear.[4]

The Queen Mary University team hypothesized that a long course of a drug blocking that same enzyme might replicate the effect in humans. If the cells were suppressed for long enough, they might quietly die off, removing the source of the hypertension.[4]

The opportunity to test this theory in humans arrived following the first clinical trials of baxdrostat for primary aldosteronism. Researchers decided to track the patients' routine follow-up measurements long after their initial course of the experimental drug had concluded.[4]

Years without active medication

The long-term results exceeded the researchers' initial expectations for a temporary pharmacological intervention. Up to two years after the patients took their last dose of baxdrostat, the primary marker of excess aldosterone production remained 99 percent lower than it was before treatment.[4]

The clinical impact on the patients' cardiovascular health was equally dramatic and sustained. On average, the participants' blood pressure sat 25 points lower than it had been at the start of the trial, despite the absence of the aldosterone-blocking drug.[4]

Nearly one in four participants achieved completely normal blood pressure readings without needing any antihypertensive medication at all. For these individuals, a condition that typically requires lifelong management had effectively been cured by a temporary drug regimen.[1][4]

Hormone levels and blood pressure metrics remained similar to, or even lower than, the measurements recorded while the patients were actively taking baxdrostat. This suggests that the underlying architecture of the disease was fundamentally altered by the extended inhibition.[2][4]

Previous studies of aldosterone synthase inhibitors generally involved much shorter treatment windows, typically lasting just 6 to 12 weeks. Because outcomes in those trials were only measured during active treatment, the potential for a lasting remission went unnoticed.[4]

The path to broader clinical use

While the initial data is highly promising, the researchers acknowledge the pragmatic limitations of their observational follow-up. The cohort was limited to 14 individuals, and a larger, controlled study is necessary to definitively prove that the drug eliminates the problematic cells.[4]

To gather that definitive evidence, the research team is currently running a larger prospective study called the ELIXIR trial. This new phase will use advanced molecular imaging of the adrenal glands to directly observe whether the aldosterone-producing cells vanish after prolonged treatment.[4]

If the ELIXIR trial confirms these early findings in a broader population, clinical guidelines for treating primary aldosteronism could shift dramatically. A finite course of medication would offer a far more accessible alternative to invasive adrenal surgery.[3][4]

Baxdrostat is already advancing through the regulatory pipeline for broader hypertension applications. The drug was approved in the United States earlier this year for patients whose high blood pressure cannot be controlled by existing medications.[1]

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In the United Kingdom, the National Institute for Health and Care Excellence is currently assessing baxdrostat for broader use. Depending on their evaluation, the medication could become available through the National Health Service as early as next year.[1]

Finding the hidden cases

The biggest hurdle to deploying this potential cure is the chronic underdiagnosis of primary aldosteronism. Despite being responsible for up to one in ten cases of high blood pressure, fewer than one percent of affected individuals are ever formally tested for the condition.[1][2]

Most patients with the disorder are simply diagnosed with essential hypertension and prescribed a cascade of standard drugs that fail to address the root cause. They spend years cycling through different medications while their blood pressure remains dangerously high.[1][3]

Identifying the condition requires specific blood tests to measure the ratio of aldosterone to renin, followed by confirmatory testing and imaging. Because the current cure requires surgery, many clinicians have historically hesitated to pursue the complex diagnostic workup.[2][4]

The prospect of a simple, pill-based cure could radically change how doctors approach treatment-resistant hypertension. If a 12-month prescription can permanently resolve the issue, widespread screening for primary aldosteronism would become a clinical imperative rather than an academic exercise.[3][4]

For the millions of people unknowingly living with this specific hormonal imbalance, the research offers a tangible horizon of hope. Medicine traditionally relies on drugs that patients must take forever, making the discovery of one they can eventually stop a rare and welcome breakthrough.[1][4]