Calcium Channel Blockers: Review of Chemistry, Biochemical Mechanisms, and Pharmacological Effects

Alkhaldi, Nasser Hassan Abdullah; Alshammari, Rikan Mashan; Alamri, Abdulelah Mohammed Mubashir; Alotaibi, Saad Obaid; Alshammariy, Yousif Fheed; Al Mutairi, Haleemah Nashi; Alsomali, Zainab Adam; Mohamed, Asma; Elyas, Mohanad Emad; Aljuhani, Maryam Awad; Alhirbish, Hanan Ahmed; Alsarimi, Fayez Abdullah Hussain; Almuhaylib, Abdulaziz Mohammed; Al-Anzi, Badr Sayyah; Al-Ahmad, Ahmed Ibrahim

doi:10.21608/ejchem.2025.401345.12007

Calcium Channel Blockers: Review of Chemistry, Biochemical Mechanisms, and Pharmacological Effects

Articles in Press

Document Type : Review Articles

Authors

National guard Prince Mohammad bin Abdul-Aziz hospital, Saudi Arabia

10.21608/ejchem.2025.401345.12007

Abstract

Background: Calcium channel blockers (CCBs) are a cornerstone in cardiovascular pharmacotherapy, widely used for hypertension, angina, and arrhythmias since their introduction in the 1970s. These drugs inhibit L-type calcium channels, reducing calcium influx in vascular smooth muscle and cardiac cells, leading to vasodilation and modulated cardiac conduction. Despite their efficacy, CCBs are associated with significant adverse effects and drug interactions, necessitating careful clinical management.

Aim: This review examines the pharmacology, therapeutic applications, and clinical challenges of CCBs, emphasizing their classification, mechanisms, pharmacokinetics, and toxicity profiles.

Methods: A comprehensive analysis of peer-reviewed literature and clinical guidelines was conducted, focusing on CCB chemistry, biochemical pathways, approved/off-label uses, and management of overdose.

Results: CCBs are categorized into dihydropyridines (e.g., amlodipine, nifedipine) and non-dihydropyridines (verapamil, diltiazem), with distinct tissue selectivity and clinical indications. Dihydropyridines primarily vasodilate, treating hypertension and angina, while non-dihydropyridines additionally suppress cardiac conduction, aiding arrhythmia management. Key adverse effects include peripheral edema (dihydropyridines) and bradycardia/AV block (non-dihydropyridines). Overdose manifests as refractory hypotension, bradycardia, and hyperglycemia, managed with calcium, vasopressors, and hyperinsulinemia-euglycemia therapy (HIE).

Conclusion: CCBs remain vital in cardiovascular therapy but require vigilant monitoring due to their narrow therapeutic index and interaction potential. Interprofessional collaboration optimizes outcomes, particularly in high-risk populations. Future research should explore safer analogs and antidotes for toxicity

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