Pharmacodynamics of Metoprolol

Beta-2-Adrenergic receptor blockers are a class of drugs used mainly in the management of hypertension, glaucoma and congestive cardiac failure. Drugs in this class are known to imitate the actions of endogenous s catecholamines. The paper seeks to explore the pharmacodynamics of metoprolol.

Question 1. Metoprolol is a cardioselective beta-1 adrenergic receptor antagonist that selectively blocks the activity of beta-1 adrenoceptors found primarily in the heart, thereby reducing heart rate and contractility. While metoprolol is selective for beta-1 receptors, it can also interact with beta-2 receptors at high doses. However, this is generally not clinically significant due to the higher affinity of metoprolol for beta-1 receptors.

Question 2. Effect of Beta 2 Antagonist on the heart: Beta- 2- Receptor antagonists reduces heart rate and myocardial contractility. By blocking the actions of the sympathetic nervous system, metoprolol can reduce the effects of stress hormones such as adrenaline and noradrenaline, leading to a decrease in blood pressure and heart rate, making it an effective treatment option for certain cardiovascular conditions (Fowler et al., 2018). This pharmacological effect decreases myocardial oxygen demand and improves cardiac efficiency, making it helpful in managing hypertension, angina pectoris, and heart failure.

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Question 3: Metabolism of Metoprolol. Metoprolol is primarily metabolized in the liver. Specifically, it undergoes extensive first-pass metabolism in the liver, primarily metabolizing it by the enzyme cytochrome P450 (CYP) 2D6 into an inactive metabolite (Thomas et al., 2020). The pharmacokinetics of metoprolol is also essential to consider, as its metabolism can be affected by other medications that may inhibit or induce CYP2D6 activity, leading to potential drug interactions and changes in metoprolol’s therapeutic effects.

Question 4. Beta-blockers can also cause bronchospasm, a narrowing of the airways in the lungs that can worsen asthma symptoms. Therefore, healthcare providers must exercise caution when prescribing beta-blockers to patients with asthma (Abosamak et al., 2022). They cause bronchoconstriction by antagonizing the effects of adrenaline on bronchial smooth muscles; ATP is not converted to cAMP failure of activation of protein kinases. The net effect is an exacerbation of symptoms of asthma which manifest as coughing or wheezing.

Pharmacodynamics of Metoprolol References

Abosamak, N. R., & Shahin, M. H. (2023). Beta 2 Receptor Agonists/Antagonists. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK559069/

Fowler, E. D., Drinkhill, M. J., Norman, R., Pervolaraki, E., Stones, R., Steer, E., Benoist, D., Steele, D. S., Calaghan, S. C., & White, E. (2018). Beta1-adrenoceptor antagonist, metoprolol attenuates cardiac myocyte Ca2+ handling dysfunction in rats with pulmonary artery hypertension. Journal of Molecular and Cellular Cardiology, 120, 74–83. https://doi.org/10.1016/j.yjmcc.2018.05.015

Thomas, C. D., Mosley, S. A., Kim, S., Lingineni, K., El Rouby, N., Langaee, T. Y., Gong, Y., Wang, D., Schmidt, S. O., Binkley, P. F., Estores, D. S., Feng, K., Kim, H., Kinjo, M., Li, Z., Fang, L., Chapman, A. B., Cooper-DeHoff, R. M., Gums, J. G., … Cavallari, L. H. (2020). Examination of Metoprolol Pharmacokinetics and Pharmacodynamics Across CYP2D6 Genotype‐Derived Activity Scores. CPT: Pharmacometrics & Systems Pharmacology, 9(12), 678–685. https://doi.org/10.1002/psp4.12563