New York
A widely-prescribed drug for treating hypertension or blood pressure called amlodipine is not dangerous for patients, a new research that included an Indian-origin scientist has shown, despite recent concerns from researchers and clinicians that taking amlodipine may have risks.
The number of adults aged 30–79 years with hypertension has increased from 650 million to 1.28 billion in the last 30 years, according to a recent global analysis of trends in hypertension prevalence led by Imperial College London and WHO that was published in The Lancet.
A new paper in the journal Function, published by Oxford University Press, has found that amlodipine drug is safe for use to treat hypertension.
“Removal of amlodipine as a front-line therapy would most likely increase deaths from hypertension dramatically,” said Anant Parekh, chief of the signal transduction laboratory at The National Institutes of Health Research in North Carolina in the US.
“The study recommends that amlodipine remain a first-line treatment for high blood pressure,” Parekh added.
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 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.
The study by research teams from National Institutes of Health and Glasgow University found 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