Beta blockers, as their name suggests, target beta receptor sites found in the sympathetic nervous system (commonly referred to as the 'fight or flight' response). Receptors of this system focus on the stimulation of the body for high-activity situations and are divided into two main sub-classes, Beta 1 and Beta 2. Beta 1 receptors are generally found in the heart. When activated, they stimulate adenylyl cyclase to form cyclic adenosine monophosphate (broken down from adenosine triphosphate, the cells' main source of energy), which in turn activates a protein which causes calcium channels in heart cells to take in more calcium. This convoluted process increases heart rate, conduction of electricity through the heart, and strengthens contractions to increase blood flow. In lungs, a different process opens up the bronchi to allow for more air passage. These receptors are activated by adrenergic agonists, either epinephrine or norepinephrine.
Beta blockers, however, are adrenergic antagonists. Beta blockers bond to the same receptor sites as the adrenergic agonists, but do not elicit the desired effects, blocking the beta receptor sites. As a result, an active individual on beta blockers may have a disproportionately low heart rate compared to an active individual without.
|Heart||Increased heart rate (Chronotropy).
|Bladder||Relaxation of detrusor muscle (diminished urge to urinate)|
|Kidneys||Releases Renin (increases blood pressure)|
|Arterioles (heart, lungs, skeletal muscle)||Vasodilation|
|Lungs||Dilation of bronchi and bronchioles (eases breathing)|
|Liver||Glycogenolysis (breakdown of glycogen into glucose)|
|Skeletal Muscle||Enhanced contraction, glycogenolysis|
Beta Blockers are divided into two sub-classes: cardio-selective and non-selective. Cardio-selective beta blockers have a stronger affinity for beta-1 receptor sites in the heart, though at higher doses will have effects similar to non-selective beta-blockers. Non-selective beta blockers will also act on beta-2 receptor sites, found in vascular and broncial smooth muscle, eyes, liver, pancreas, gastrointestinal tract, and uterus. Some beta blockers also possess intrinsic sympathomimetic activity, only partially blocking beta receptors, resulting in a diminished reduction in heart rate, cardiac output, and blood pressure.
Cardio-Selective Beta Blockers (Primarily Beta 1)
- Acebutolol, Atenolol, Bisoprolol, Metoprolol
Non-Selective Beta Blockers (All Beta Receptors)
- Carvedilol, Labetalol, Nadolol, Pindolol, Propranolol, Sotalol, Timolol
Calcium Channel Blockers
Non-dihydropyridines work in the cardiac conductive cells, targeting the calcium ion channels. These channels open to take in calcium, causing a rapid rise in voltage that allows conductive cells to send out the signal for contractile cells to contract. Calcium channel blockers slow the rate that calcium enters cells, increasing the time it takes for the voltage to rise to the needed level and decreasing the rate at which the heart can send out pulses and contract.
Dihydropyridines work on the calcium channels in vascular muscle, though some have a limited effect in the cardiac conductive cells. The patient's peripheral vascular system dilates, causing a decrease in blood pressure.
For another explanation, see the Khan Academy’s video on anti-arrhythmic medications: https://www.youtube.com/watch?v=5xSEZszGDtI. (The Beta Blocker Section begins at 06:20, and the Calcium Channel Blocker section begins at 10:00).
Side effects of beta blocker medication is largely related to the cardiac effects of the drugs and can include fatigue, headache, dizziness, hypotension, nausea, and bradycardia. It is important to note that most side effects appear shortly after the patient begins beta blocker therapy, changes medications, or changes doses. In patients with long-term beta-blocker therapy, side effects should be rare and well-managed.
Calcium channel blocker side effects are similarly cardiac in nature. Dizziness, lightheadedness, headache, and fainting can occur due to drops in blood pressure. Dihydropyridines can cause swelling of the extremities (peripheral edema) as a result of capillary vasodilation. Since beta receptors and cardiac calcium channels are not blocked with dihydropine calcium channel blocker therapy, the heart may increase in speed (compensatory tachycardia) and force, as the body attempts to balance out the vasodilation and resulting drop in blood pressure. Calcium channel blockers affect coagulation by slightly diminishing platelet aggregation.
Compendium of Pharmaceuticals and Specialties, online version (CPS). Beta-adrenergic Blocking Agents. Last Revised February 2014. © Canadian Pharmacists Association, 2015. All rights reserved.
Compendium of Pharmaceuticals and Specialties, online version (CPS). Calcium Channel Blockers. Last Revised September 2011. © Canadian Pharmacists Association, 2015. All rights reserved.
Various authors. (2017).Anatomy & Physiology. Houston, TX: OpenStax. Retrieved from https://d3bxy9euw4e147.cloudfront.net/oscms-prodcms/media/documents/AnatomyandPhysiology-OP.pdf.
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