Calcium Channel Blockers: Review of Chemistry, Biochemical Mechanisms, and Pharmacological Effects | ||
| Egyptian Journal of Chemistry | ||
| Volume 68, Issue 13, December 2025, Pages 641-650 PDF (300.26 K) | ||
| Document Type: Review Articles | ||
| DOI: 10.21608/ejchem.2025.401345.12007 | ||
| Authors | ||
| Nasser Hassan Abdullah Alkhaldi* ; Rikan Mashan Alshammari; Abdulelah Mohammed Mubashir Alamri; Saad Obaid Alotaibi; Yousif Fheed Alshammariy; Haleemah Nashi Al Mutairi; Zainab Adam Alsomali; Asma Mohamed; Mohanad Emad Elyas; Maryam Awad Aljuhani; Hanan ahmed Alhirbish; Fayez Abdullah Hussain Alsarimi; Abdulaziz Mohammed Almuhaylib; Badr Sayyah Al-Anzi; Ahmed Ibrahim Al-Ahmad | ||
| National guard Prince Mohammad bin Abdul-Aziz hospital, Saudi Arabia | ||
| 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 | ||
| Keywords | ||
| Calcium channel blockers; dihydropyridines; non-dihydropyridines; hypertension; arrhythmias; CCB toxicity | ||
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