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Cardiovascular Physiology Concepts on Nitric Oxide

2012 dianna

Nitric Oxide is often referred to as (NO):

  • Conditions or Diseases Connected with Unusual Nitric Oxide Creation and Bioavailability
  • Intracellular Mechanisms
  • Nitric Oxide Biosynthesis
  • Vascular Effects of Nitric Oxide

Nitric oxide (NO) is created by lots of cells in the body; nonetheless, its creation by vascular endothelium is specifically crucial in the management of blood circulation. Due to the fact that of its significance in vascular function, irregular manufacturing of Nitric Oxide, as takes place in various disease states, can negatively impact blood circulation and various other vascular functions.


Nitric Oxide Biosynthesis

Nitric Oxide is created from the amino acid L-arginine by the enzymatic activity of nitric oxide synthase (NOS). There are 2 endothelial kinds of NOS: essential NOS (cNOS; type III) and inducible NOS (iNOS; type II). Co-factors for NOS include flavin adenine nucleotides, NADPH. oxygen, tetrahydrobiopterin.

Under regular, basal conditions in blood vessels, Nitric Oxide is constantly being created by cNOS. The action of cNOS is calmodulin and calcium dependent. There are 2 fundamental pathways for the stimulation of cNOS, both of which involve release of calcium ions from subsarcolemmal storage sites.

Shearing forces acting on the vascular endothelium produced by blood circulation triggers a launch of calcium and succeeding cNOS activation. Increases in blood flow stimulate Nitric Oxide formation (flow-dependent Nitric Oxide formation).


Nitric Oxide formation

Next, endothelial receptors for a difference of ligands encourage calcium release and following Nitric Oxide production (receptor-stimulated Nitric Oxide formation). Receptors are built in for acetylcholine, adenosine, bradykinin, substance-P, adenosine, and many others vasoactive substances.

In the 1970s, Dr. Robert Furchgott noted that acetylcholine launched a compound that produced vascular relaxation, however just when the endothelium was undamaged. This scrutiny unlocked this field of research and finally led to his accepting a Nobel prize. At first, Furchgott labeled this element endothelium-derived relaxing factor (EDRF), but by the mid-1980’s he and others discovered this substance as being Nitric Oxide (NO).

The various other isoform of endothelial NOS is iNOS. Under common, initial conditions, the activity of iNOS is extremely low. The liveliness of iNOS is intensified during inflammation by bacterial endotoxins (e.g., lipopolysaccharide) and cytokines such as tumor necrosis factor (TNF) and interleukins. When there is inflammation, the quantity of Nitric Oxide produced by iNOS could be a 1,000-fold higher than that created by cNOS.


Intracellular Mechanisms

When Nitric Oxide is produced, it has a half-life period of just a few seconds, mainly because superoxide anion has a high affinity for Nitric Oxide (both molecules have an unpaired electron making them highly reactive). For that reason, superoxide anion decreases Nitric Oxide bioavailability.

Nitric Oxide also enthusiastically binds to the heme moiety of hemoglobin (in red blood cells) and the heme moiety of the enzyme guanylyl cyclase, which is discovered in vascular smooth muscle cells and abundant additional cells of the anatomy.

When Nitric Oxide is produced by vascular endothelium, it quickly diffuses into the blood where it binds to hemoglobin and consequently broken down. It additionally diffuses into the vascular smooth muscle cells nearby to the endothelium where it binds to and triggers guanylyl cyclase.


Cyclic GMP causes smooth muscle relaxation by numerous systems consisting of:

  • enhanced intracellular cGMP, which prevents calcium entry into the cell, and reduces intracellular calcium concentrations
  • activates K+ channels, which brings about hyper-polarization and relaxation
  • activates a cGMP-dependent protein kinase that triggers myosin light chain phosphatase, the enzyme that dephosphorylates myosin light chains, which brings about smooth muscle relaxation

Due to the fact that of the main job of cGMP in Nitric Oxide mediated vasodilation, medicines (e.g., Viagra ®) that prevent the breakdown of cGMP (cGMP-dependent phosphodiesterase inhibitors) are utilized to boost Nitric Oxide mediated vasodilation, specifically in penile erectile cells in the therapy of impotence. Enhanced cGMP also has an essential anti-platelet, anti-aggregatory result.

  • Vascular Effects of Nitric Oxide
  • Vascular activities of Nitric Oxide consist of the following:
  • Anti-inflammatory impact - prevents leukocyte adhesion to vascular endothelium; scavenges superoxide anion
  • Anti-proliferative impact - inhibits smooth muscle hyperplasia
  • Anti-thrombotic impact - prevents platelet adhesion to the vascular endothelium
  • Direct vasodilation (circulation reliant and receptor moderated)
  • Roundabout vasodilation by preventing vasoconstrictor impacts (e.g., hinders angiotensin II and sympathetic vasoconstriction)


Due to the fact that of the above activities of Nitric Oxide, when its manufacturing is hindered or its bioavailability is lowered, the following can result:

  • Aging, Ageing
  • Atherosclerosis
  • Cigarette smoking
  • Diabetes (both kind I and II)
  • Diseases or conditions Associated with Abnormal Nitric Oxide Production and Bioavailability
  • Dyslipidemias is an abnormal amount of lipids (specifically hypercholesterolemia and hypertriglyceridemia)
  • Heart failure
  • Hypertension
  • Inflammation due to up-regulation of leukocyte and endothelial adhesion molecules
  • Obesity
  • Thrombosis due to platelet aggregation and adhesion to vascular endothelium
  • Vascular hypertrophy and stenosis
  • Vasoconstriction (e.g., coronary vasospasm, high systemic vascular resistance, high blood pressure)



Keywords: Cardiovascular, Physiology Concepts, Nitric Oxide, Nitric Oxide (NO), Diseases Connected with Unusual Nitric Oxide Creation and Bioavailability, Intracellular Mechanisms, Nitric Oxide Biosynthesis, Vascular Effects of Nitric Oxide, vascular endothelium, blood circulation, Nitric Oxide Biosynthesis, L-arginine, arginine, nitric oxide synthase, (NOS), Dr. Robert Furchgott, acetylcholine, aging, ageing, Nobel prize, inflammation, cGMP, Vascular, Anti-inflammatory, superoxide anion, Atherosclerosis, Cigarette smoking, Diabetes, Heart failure, Hypertension, obesity, Thrombosis, platelet aggregation, vascular endothelium, Vascular hypertrophy, stenosis, Vasoconstriction, high blood pressure

DISCLAIMER: These products are for academic functions only, and are not a source of medical decision-making recommendations.



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PRIME Nitric Oxide Activator contains L-citrulline, which converts to L-arginine in the body. Researchers have suggested and reported that L-arginine made from L-citrulline is much more effective at raising NO levels than taking L-arginine directly.
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