How do beta blockers (beta-adrenergic blocking agents) prevent exposure to catecholamines?

From the Guidelines

Beta-blockers do not prevent exposure to catecholamines, but rather block the effects of these catecholamines at beta-adrenergic receptors. Beta-blockers work by competitively binding to beta-receptors in various tissues, preventing catecholamines from activating these receptors 1. This mechanism is crucial in reducing myocardial oxygen demand, which is a key factor in managing patients with unstable angina or non-ST-elevation myocardial infarction.

Key Points

• Beta-blockers reduce myocardial oxygen demand by inhibiting the effects of catecholamines on beta-1 adrenergic receptors, primarily located in the myocardium 1.
• The benefits of beta-blockers include reducing heart rate, blood pressure, and cardiac output, which are essential in managing patients with myocardial infarction 1.
• Common beta-blockers used in clinical practice include metoprolol, propranolol, and atenolol, with dosages varying depending on the specific clinical scenario 1.
• Beta-blockers are classified as non-selective or cardioselective, which determines their specific effects and side effect profiles 1.
• The body continues to produce and release catecholamines normally; beta-blockers simply prevent the target tissues from responding to them 1.

Clinical Implications

• Beta-blockers should be initiated orally in patients with unstable angina or non-ST-elevation myocardial infarction, in the absence of contraindications, within the first 24 hours 1.
• The choice of beta-blocker should be based on pharmacokinetic and side effect criteria, as well as physician familiarity, with a preference for agents without intrinsic sympathomimetic activity 1.
• In patients with myocardial infarction complicated by systolic cardiomyopathy or heart failure, one of the three proven beta-blockers (carvedilol, sustained-release metoprolol succinate, or bisoprolol) should be used 1.

From the FDA Drug Label

The FDA drug label does not answer the question.

From the Research

Mechanism of Action

• Beta-blockers prevent exposure to catecholamines by antagonizing β-adrenergic receptors (ARs) 2, which belong to the G protein-coupled receptor family and receive their stimulus from endogenous catecholamines.
• Upon β-AR stimulation, numerous intracellular cascades are activated, ultimately leading to cardiac contraction or vascular dilation, depending on the relevant subtype and their location 2.
• Beta-blockers are able to block β1-, β2-, and β3-ARs, with β1 being the most abundant subtype in the heart 2.

Types of Beta-Blockers

• There are three generations of beta-blockers: nonselective β-blockers, cardioselective β-blockers (selective β1-antagonists), and a third generation of these drugs able to block β1 together with extra vasodilation activity 2.
• Beta-blockers can be used in combination with other anti-hypertension drugs to achieve maximal blood pressure control 3.
• The choice of beta-blocker is important, as benefit is not a class-effect, and some beta-blockers (e.g. xamoterol, bucindolol, nebivolol) have intrinsic sympathomimetic activity (ISA) that diminishes efficacy 4.

Clinical Applications

• Beta-blockers are widely used in the treatment of cardiovascular diseases, including hypertension, heart failure, and coronary artery disease 4, 3, 5.
• Beta-blockers can reduce the risk of heart failure by inhibiting chronic beta-1 stimulation-induced myocardial apoptosis/necrosis/inflammation 4.
• Beta-blockers may be useful in patients with hyperkinetic circulation, migraine headache, and essential tremor 3.