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Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

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Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
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Third-generation β-blockers, such as labetalol and carvedilol, represent a significant advancement in managing cardiovascular conditions. Unlike conventional β-blockers, which can induce peripheral vasoconstriction, third-generation drugs block α1 adrenoceptors. This promotes vasodilation through several mechanisms, such as increased nitric oxide production, inhibition of calcium ion entry, opening of potassium ion channels, and antioxidant action. Labetalol, for instance, is...
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Local Anesthetics: Adverse Effects01:12

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While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
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Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
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Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
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Related Experiment Video

Updated: Mar 13, 2026

A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
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Amlodipine-Induced Gingival Overgrowth.

R Jayanthi1, P Boopathi Rajan2

  • 1Professor.

The Journal of the Association of Physicians of India
|October 13, 2016
PubMed
Summary

Gingival overgrowth, a side effect of some medications, is rarely linked to amlodipine. This report details four hypertension patients experiencing this rare amlodipine-induced gingival overgrowth.

Area of Science:

  • Pharmacology
  • Periodontology
  • Drug-induced diseases

Background:

  • Gingival overgrowth is a known side effect of certain medications, including anticonvulsants (e.g., phenytoin), immunosuppressants (e.g., cyclosporine), and calcium channel blockers (e.g., nifedipine).
  • Nifedipine, a calcium channel blocker, is associated with gingival overgrowth in approximately 10% of patients.
  • Gingival overgrowth induced by amlodipine, another calcium channel blocker, is considered very limited in occurrence.

Observation:

  • This study reports on four hypertensive patients who developed gingival overgrowth.
  • The patients were undergoing treatment with amlodipine.

Findings:

  • The four cases presented demonstrate that amlodipine can indeed cause gingival overgrowth, contrary to its limited reported incidence.

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  • This suggests a potential underreporting or a specific patient susceptibility to amlodipine-induced gingival overgrowth.

    • Implications:

    • These findings highlight the importance of monitoring for gingival overgrowth in patients taking amlodipine, particularly those with hypertension.
    • Clinicians should consider amlodipine as a potential etiological factor for gingival overgrowth.
    • Further research is warranted to elucidate the mechanisms and prevalence of amlodipine-induced gingival overgrowth.