[Calcium antagonists: current and future applications based on new evidence. Neuroprotective effect of calcium

Yasuo Ito1, Nobuo Araki

  • 1Department of Neurology, Faculty of Medicine, Saitama Medical University, Japan.

Clinical Calcium
|January 6, 2010
PubMed

Insights

Calcium channel blockers show neuroprotective effects. Cilnidipine and amlodipine reduce brain damage, while omega-conotoxin prevents neuronal cell death, suggesting therapeutic potential for calcium antagonists.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cardiovascular Research

Context:

  • Voltage-dependent calcium channels are crucial for neuronal function and have diverse subtypes (L-, N-, T-, P-, and Q-type).
  • Cerebral ischemia and neuronal cell death are significant challenges in neurological disorders.
  • Calcium channel blockers are established treatments for cardiovascular conditions.

Purpose:

  • To investigate the neuroprotective effects of specific calcium channel blockers.
  • To evaluate the impact of L/N-type, L-type, and N-type calcium channel blockers on cerebral infarction and neuronal survival.

Summary:

  • Cilnidipine (L/N-type Ca2+ channel blocker) reduced cerebral infarction size in a rat model of focal brain ischemia.
  • Amlodipine (L-type Ca2+ channel blocker) demonstrated efficacy in reducing cerebral edema and inhibiting neuronal cell death.
  • Omega-conotoxin (N-type Ca2+ channel blocker) decreased cerebral infarction size and prevented delayed neuronal death in the hippocampus.

Impact:

  • These findings suggest that calcium antagonists possess significant neuroprotective properties.
  • Targeting specific calcium channel subtypes may offer novel therapeutic strategies for stroke and other neurological injuries.
  • Further research into calcium channel modulation could lead to improved treatments for brain damage.

Related Concept Videos

Antiepileptic Drugs: Calcium Channel Blockers01:17

Antiepileptic Drugs: Calcium Channel Blockers

Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

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.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

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,...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...