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Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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...
Adrenergic Antagonists: ɑ and β-Receptor Blockers01:31

Adrenergic Antagonists: ɑ and β-Receptor Blockers

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 clinically...

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Related Experiment Video

Updated: May 17, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Reinventing amlodipine.

Bartosz Grzymala1, Dagmar Þöll Halldórsdóttir1, Haraldur Þorsteinsson1

  • 13Z, Reykjavik, Iceland.

The Journal of Pharmacology and Experimental Therapeutics
|May 15, 2026
PubMed
Summary
This summary is machine-generated.

This review suggests amlodipine, a calcium channel blocker, may be a novel therapeutic for attention-deficit/hyperactivity disorder (ADHD). Preclinical and genetic evidence supports its potential, with S-amlodipine being the preferred form for ADHD treatment.

Keywords:
AmlodipineAttention-deficit/hyperactivity disorderDopamineDrug repurposingS-amlodipinel-type calcium channels

Related Experiment Videos

Last Updated: May 17, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
07:24

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR

Published on: April 8, 2013

Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Attention-deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder with limited pharmacological treatment specificity.
  • Current non-stimulant ADHD medications primarily target noradrenergic systems with modest efficacy.
  • l-Type calcium channels (LTCCs) play crucial roles in neuronal function and are implicated in ADHD pathophysiology.

Purpose of the Study:

  • To evaluate the potential of repurposing the LTCC blocker amlodipine as a novel therapeutic for ADHD.
  • To propose a mechanistic framework for amlodipine's action in ADHD-relevant circuits.
  • To highlight amlodipine's potential to address therapeutic avenues not covered by existing ADHD treatments.

Main Methods:

  • Review of existing evidence on amlodipine's effects on LTCCs and its relevance to ADHD.
  • Analysis of preclinical findings in animal models of ADHD (zebrafish and rats).
  • Examination of biobank data correlating amlodipine use with ADHD traits in at-risk individuals.

Main Results:

  • Amlodipine penetrates the blood-brain barrier, contrary to previous assumptions.
  • Preclinical studies demonstrated phenotype rescue and normalization of metabolic pathways in ADHD models.
  • Biobank analyses indicated reduced ADHD traits in individuals taking amlodipine.
  • S-amlodipine exhibits higher LTCC affinity and fewer off-target effects compared to R-amlodipine.

Conclusions:

  • Genetic, preclinical, and translational evidence supports LTCC modulation via amlodipine for ADHD.
  • S-amlodipine is identified as the rational candidate for ADHD therapeutic development due to its specific pharmacology.
  • Further research, including clinical trials, is warranted to establish amlodipine's efficacy and safety for ADHD treatment.