Atenolol is a β1 receptor selective antagonist, a drug belonging to the group of β-blockers, a class of drugs used primarily in cardiovascular diseases. Introduced in 1976, atenolol was developed as a replacement for propranolol in the treatment of hypertension. The chemical works by slowing down the heart and reducing its workload. Unlike Propranolol, atenolol does not pass through the blood-brain barrier thus avoiding various CNS side effects.[1]
Whilst atenolol, the most widely used β-blocker in the United Kingdom, was once first-line treatment for hypertension, the role for β-blockers in hypertension was downgraded in June 2006 in the United Kingdom to fourth-line as they perform less well than other drugs, particularly in the elderly, and there is increasing evidence that the most frequently used β-blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.[2]
Whilst atenolol, the most widely used β-blocker in the United Kingdom, was once first-line treatment for hypertension, the role for β-blockers in hypertension was downgraded in June 2006 in the United Kingdom to fourth-line as they perform less well than other drugs, particularly in the elderly, and there is increasing evidence that the most frequently used β-blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.[2]
Side effects
Atenolol causes significantly fewer central nervous system side effects (depressions, nightmares) and fewer bronchospastic reactions, both due to its particular pharmacologic profile.
It was the main β-blocker identified as carrying a higher risk of provoking type 2 diabetes, leading to its downgrading in the United Kingdom in June 2006 to fourth-line agent in the management of hypertension.[2]
In addition, β-blockers blunt the usual sympathetic nervous system response to hypoglycemia (i.e. sweating, agitation, tachycardia). These drugs therefore have an ability to mask a dangerously low blood sugar, which further decreases their safety and utility in diabetic patients
It was the main β-blocker identified as carrying a higher risk of provoking type 2 diabetes, leading to its downgrading in the United Kingdom in June 2006 to fourth-line agent in the management of hypertension.[2]
In addition, β-blockers blunt the usual sympathetic nervous system response to hypoglycemia (i.e. sweating, agitation, tachycardia). These drugs therefore have an ability to mask a dangerously low blood sugar, which further decreases their safety and utility in diabetic patients
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