Related Experiment Video

Updated: Jun 22, 2026

Use of a Hanging Weight System for Coronary Artery Occlusion in Mice
08:30

Use of a Hanging Weight System for Coronary Artery Occlusion in Mice

Published on: April 19, 2011

The role of nitric oxide in A3 adenosine receptor-mediated cardioprotection

A Hussain1, P Karjian, H Maddock

  • 1Department of Biomolecular Sciences, Faculty of Health and Life Sciences, Coventry University, Coventry CV1 5FB, UK.

Autonomic & Autacoid Pharmacology
|July 2, 2009
PubMed

Insights

This review explores how A3 adenosine receptors and nitric oxide pathways can protect the heart from cell death after ischemia and reperfusion injury. These findings may lead to novel therapies for reducing heart attack damage.

Area of Science:

  • Cardiology
  • Pharmacology
  • Cell Biology

Background:

  • Ischemia reperfusion-related cell death significantly contributes to global heart mortality.
  • Coronary heart disease (CHD) causes over 100,000 deaths annually in the UK, with millions affected by angina or myocardial infarction.
  • Current reperfusion treatments like thrombolysis and angioplasty have limitations, highlighting the need for new strategies to minimize infarct size.

Purpose of the Study:

  • To review intracellular signaling pathways linked to A3 adenosine receptors for reducing post-ischemic infarct size.
  • To discuss the specific role of nitric oxide in A3 adenosine receptor-mediated cardioprotection.

Main Methods:

  • Literature review of studies investigating A3 adenosine receptors and cardioprotection.
  • Focus on intracellular signaling mechanisms, particularly involving nitric oxide.

Main Results:

  • A3 adenosine receptors are implicated in intracellular signaling pathways that can reduce infarct size.
  • Nitric oxide plays a crucial role in the cardioprotective effects mediated by A3 adenosine receptors.

Conclusions:

  • Targeting A3 adenosine receptors and associated nitric oxide pathways presents a promising therapeutic strategy for limiting ischemia reperfusion injury.
  • Further research into these pathways could lead to novel treatments for reducing heart damage after myocardial infarction.

More Related Videos

Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice07:55

Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice

Published on: May 5, 2011

Related Concept Videos

Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
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...
Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
Cardiopulmonary Resuscitation III: AED Use01:23

Cardiopulmonary Resuscitation III: AED Use

Introduction to AEDAn Automated External Defibrillator (AED) is a portable medical device that analyzes the heart's rhythm and, if necessary, delivers an electrical shock to help the heart re-establish an effective rhythm during sudden cardiac arrest (SCA). SCA occurs when the heart suddenly and unexpectedly stops beating, leading to a loss of blood flow to the brain and other vital organs. In such emergencies, time is of the essence, and using an AED, combined with Cardiopulmonary...