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Home»Health»Common blood pressure drug slows aging, even in older animals
Health

Common blood pressure drug slows aging, even in older animals

u1news-staffBy u1news-staffFebruary 24, 2026No Comments5 Mins Read
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Blood pressure drug rilmenidine extends life slows aging animals 1m.jpg
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Today, many people are living longer than their parents or grandparents, but those extra years often come with chronic illnesses. Scientists want the next few decades to feel more like prime time than overtime, and are looking for ways to slow the biological slide that typically accelerates after age 65.

One method that’s getting serious attention replaces crash dieting with chemistry.



calorie cut Without malnutrition, mice, earthworms, and even rhesus macaques can live longer, but sticking to that routine can be difficult and can lead to dizziness, brittle bones, and thinning hair.

Researchers are looking for a pill that would have the same effect while leaving dinner on the plate.

The importance of aging research

Most of the major causes of death are due to aging – heart disease, cancer, dementia – By forcing cells into dysfunction. By slowing the underlying process, we may be able to reduce the burden of multiple symptoms at once, rather than treating them individually.

Public health economists say that reducing late-life disability by even a few years could save billions of dollars in long-term care costs and improve the quality of life for millions of people.

While most drug discovery still targets single diseases, a growing field called geriatrics treats aging itself as the root cause.

Calorie restriction mimetics (CRMs) are high on wish lists. metabolic circuit Animals are already using it to survive times of famine.

When these circuits are turned on, cells repair damaged proteins, improve energy use, and strengthen stress defenses.

Calorie restriction and its hurdles

classic calorie restriction This usually means consuming 20 to 40 percent fewer calories than usual for many years.

Although the evidence in rodents is surprising, people feel that this therapy is unsustainable and that extreme energy reduction can weaken immunity. Safer strategies aim to flip the same molecular switch through drug therapy.

Currently, computational screening tools search drug libraries for compounds that cause human cells to mimic the gene expression profile seen under caloric deficit.

This approach is faster than testing each molecule in live animals first and often focuses on drugs already approved for other conditions, cutting the path to clinical trials by years.

Rilmenidine – a common drug that fights aging

One surprising hit in these searches is rilmenidine. high blood pressure medicine It has been taken orally for 30 years.

After a machine learning model flagged the problem, a team led by molecular biogerontologist João Pedro Magalhães University of Birmingham, UK put it to the test Caenorhabditis elegansa small soil insect favored by older researchers.

“For the first time in animals, we can demonstrate that rilmenidine can extend lifespan,” he said.

The same exam brought another bonus. Elderly nematodes were almost as effective as young worms, suggesting that humans do not need to start treatment until middle age.

Drug safety records are also helpful. Doctors around the world prescribe rilmenidine for high blood pressure, but side effects are rare and relatively mild. In rare cases, symptoms such as palpitations, insomnia, and drowsiness may occur.

As Dr. Magalhães stated, “We are now keen to study whether rilmenidine can be translated into other clinical uses.”

How rilmenidine works inside cells

Rilmenidine binds to imidazoline receptors, small docking stations on cell membranes that regulate metabolism. In C. elegans there is one receptor called . Nishi-1 It turned out to be essential.

“We found that when nish-1 was deleted, the lifespan-extending effect of rilmenidine was abolished,” the researchers explained. They then reintroduced the receptor gene. Restoring nish-1 receptors reversed the increase in lifespan after treatment with rilmenidine.

These findings outline clear paths for future drug adjustments aimed at increasing efficacy or reducing undesirable effects.

Downstream of nish-1, treated worms had enhanced autophagy, the cellular waste disposal system, and tolerated heat stress better than untreated worms.

Neither developmental timing nor fertility was altered, suggesting that the drug targeted aging pathways rather than growth or reproduction.

Cross-species testing

C.Elegance share many genes But researchers need data from mammals before moving on to humans.

Therefore, the Birmingham research group gave mice rilmenidine and observed changes in gene expression in liver and kidney tissue that were consistent with the hallmarks of classical calorie restriction.

Blood biomarkers of metabolism shifted to more youthful levels, reinforcing the idea that the pill taps into an ancient survival program that is conserved across species.

Because this compound is already approved, early-stage human clinical trials can focus directly on biological markers such as: inflammatory proteininsulin sensitivity, and muscle strength.

Oral delivery of rilmenidine has practical advantages over drugs that require injections or special diets.

Rilmenidine and the future of anti-aging

Long-term human studies will need to rule out subtle harms and confirm that improved markers translate into healthier years. Still, experts see momentum building.

“As the world’s population continues to age, the benefits of slowing aging, even slightly, are enormous,” Magalhães said.

Regulators will need new guidelines for drugs that target aging rather than diagnosed diseases, and ethicists are debating fair access. But it’s hard to ignore the possibility of taking a small pill every day instead of counting every calorie.

If rilmenidine or similar compounds continue to prove safe and effective, the next generation of older adults may find that staying healthy into their 80s will feel less like luck and more like routine science.

The entire study was published in the journal aged cells.

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