In a study published in Neuropsychopharmacology, researchers tested five potential drugs in rats bred to exhibit ADHD-like symptoms. Among them, only amlodipine, a common blood pressure medication, significantly reduced hyperactivity.

To confirm its effects the team tested amlodipine in zebrafish, an important model for studying brain function sharing about 70% of genes with humans. The results showed that amlodipine also reduced hyperactivity and impulsivity—core symptoms of ADHD—in these fish. Further analysis of the fish revealed that amlodipine crosses the blood-brain barrier for the first time, meaning it can directly influence brain function.

The researchers then turned to human genetic data and found that, remarkably, ADHD is linked to the same calcium channels in the brain as the targets for amlodipine. This suggests a potential target brain pathway for treatments. Finally, an analysis of UK-wide patient data showed that people taking amlodipine reported fewer mood swings and less risk-taking behaviour, further supporting its potential as a new ADHD treatment.

Dr Matthew Parker, co-author of the study from the University of Surrey, said:

“Repurposing amlodipine, a well-established blood pressure medication, offers a promising and swift pathway to address ADHD symptoms. Our research indicates that, due to its existing approval and safety profile, amlodipine could be rapidly redeployed as a treatment option for ADHD, potentially providing relief to patients sooner than developing new medications.”

Current ADHD medications are effective but come with significant side effects: from appetite loss, high blood pressure, headaches and sleep disturbance and carry a risk of misuse. Amlodipine, which is already widely used and well-tolerated, could offer a new, safer treatment option for ADHD.

Around 25% of patients do not respond well to any current ADHD medication, highlighting the urgent need for new treatment options.

Approximately 700,000 Americans die from hypertension each year and researchers believe some 116 million Americans (and one in five adults worldwide) have the disease, which is responsible for 7.6 million deaths per year. If untreated, hypertension significantly increases the risk of premature death through heart attack, stroke, or kidney disease.

One widely prescribed drug for treating hypertension is amlodipine, now taken regularly in pill form by over 70 million Americans. Amlodipine inhibits a type of calcium channel that is found on blood vessels. When the calcium channel opens, calcium enters the muscle and causes it to constrict, increasing blood pressure. Amlodipine prevents calcium from coming in, leading to vessel relaxation and a decrease in blood pressure.

Recently some researchers have questioned the benefit of amlodipine for treating hypertension. Studies suggested that amlodipine may activate a different type of calcium channel, resulting in changes to blood vessels and an increase in heart failure in patients. Removing amlodipine as a prescribed anti-hypertensive medication carries significant health implications, since hypertension is such a common health condition.

A new study by research teams from National Institutes of Health and Glasgow University finds that taking amlodipine is unlikely to result in an increase in heart failure in patients. The researchers found that amlodipine appears to have unique chemical properties that caused the drug to mimic the calcium channel activation, without in fact opening the channels as clinicians worried. When the study’s authors controlled for these chemical properties, they found that amlodipine did not activate calcium channels. A meta-analysis combining clinical trials and a prospective real-world analysis both showed that amlodipine was not associated with increased heart failure or other cardiovascular problems.

“Removal of amlodipine as a front-line therapy would most likely increase deaths from hypertension dramatically,” said Anant Parekh, one of the study’s authors. “The study recommends that amlodipine remain a first-line treatment for high blood pressure.”

The paper, “A reappraisal of the effects of L-type Ca2+ channel blockers on store-operated Ca2+ entry and heart failure,” is available (at midnight on October 12^th) at: https://doi.org/10.1093/function/zqad047.