Beta-blockers in the Treatment of Hypertension

Original Editor - Travis Isaac Top Contributors - Travis Isaac, Kim Jackson and Lucinda hampton

Introduction - Pharmacodynamics

The main mechanism behind which beta blockers exert their effect is by the reduction of cardiac output through lowering of the heart rate.

Beta blockers bind selectively to β-adrenoceptors, acting as competitive antagonists.[1] β1-adrenergic receptors are located primarily in the heart and kidneys and when stimulated cause cardiac muscle contraction as well as water and salt reabsorption. β2-adrenergic receptors are located primarily in the bronchial musculature and vascular smooth muscle. When stimulated, β2-adrenergic receptors cause bronchial dilation and blood vessel constriction, except in skeletal muscle.[2]

The three subclasses of beta blockers are

  • Non-vasodilating with β1-selectivity,
  • Non-vasodilating without β1-selectivity
  • Vasodilating.[3]

Beta blockers with a β1-selectivity tend to target the β1 receptor over the β2 receptor; however, their selectivity is dose-dependent and will diminish at higher doses. Beta blockers without β1-selectivity are classified as non-selective and target both the β1 and β2 adrenergic receptor.[1]

In addition, several beta blockers also act on the peripheral vasculature causing vasodilation.[3] Beta blocker induced vasodilation is mediated by the blockade of α1-adrenergic receptors, stimulation of β2-adrenergic receptors, or other mechanisms independent of adrenergic antagonism.[1]



The pharmacokinetics of beta blockers is dependent on their classification. Lipophilic drugs are quickly and completely absorbed from the gastrointestinal tract and metabolized in the gut wall and liver. Lipophilic drugs have a short half-life, typically 1-5 hours, and they easily enter the central nervous system. Whereas hydrophilic drugs are incompletely absorbed from the gastrointestinal tract and are excreted by the kidneys. Hydrophilic drugs have longer half-lives than lipophilic drugs, generally 6-24 hours and scarcely cross the blood brain barrier. Dosages for the treatment of hypertension vary depending on the drug and are typically administered orally, once or twice daily.[1]

Adverse Effects

The most severe adverse effect of beta blockers is extreme bradycardia and AV node block.[1] Clinicians must be aware that normal cardiac responses to exercise will be diminished and the typical increase in heart rate and cardiac output will be reduced.

As beta blockers reduce blood pressure, an often-seen side effect is orthostatic hypotension.[5]

Non-selective beta blockers should be avoided in patients with asthma and reactive airway disease.[6]

Beta blockers have also been shown to worsen glucose intolerance and mask the symptoms of hypoglycemia, hence caution should be used in patients with insulin-dependent diabetes.[6]

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  1. 1.0 1.1 1.2 1.3 1.4 López-Sendón J, Swedberg K, McMurray J, et al. Expert consensus document on β-adrenergic receptor blockers: The Task Force on Beta-Blockers of the European Society of Cardiology. European Heart Journal. 2004;25(15):1341-1362. doi:10.1016/j.ehj.2004.06.002
  2. Poirier L, Tobe SW. Contemporary use of β-blockers: Clinical relevance of subclassification. Canadian Journal of Cardiology. 2014;30(5):S9-S15. doi:10.1016/j.cjca.2013.12.001
  3. 3.0 3.1 Laurent S. Antihypertensive drugs. Pharmacological Research. 2017;124:116-125. doi:10.1016/j.phrs.2017.07.026
  4. Living with Heart Failure - Beta Blockers Available from: (last accessed 17.6.2019)
  5. Arnold AC, Shibao C. Current concepts in orthostatic hypotension management. Current Hypertension Reports. 2013;15(4):304-312. doi:10.1007/s11906-013-0362-3
  6. 6.0 6.1 Frishman WH, Saunders E. β-Adrenergic blockers. The Journal of Clinical Hypertension. 2011;13(9):649-653. doi:10.1111/j.1751-7176.2011.00515.x