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American Heritage Dictionary:
nitric oxide |
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Britannica Concise Encyclopedia:
nitric oxide |
For more information on nitric oxide, visit Britannica.com.
McGraw-Hill Science & Technology Encyclopedia:
Nitric oxide |
An important messenger molecule in mammals and other animals. It can be toxic or beneficial, depending on the amount and where in the body it is released. Initial research into the chemistry of nitric oxide (NO) was motivated by its production in car engines, which results in photochemical smog and acid rain. In the late 1980s, researchers in immunology, cardiovascular pharmacology, neurobiology, and toxicology discovered that nitric oxide is a crucial physiological messenger molecule. Nitric oxide is now thought to play a role in blood pressure regulation, control of blood clotting, immune defense, digestion, the senses of sight and smell, and possibly learning and memory. Nitric oxide may also participate in disease processes such as diabetes, stroke, hypertension, impotence, septic shock, and long-term depression. See also Immunology.
Most cellular messengers are large, unreactive biomolecules that make specific contacts with their targets. In contrast, nitric oxide is a small molecule that contains a free radical—that is, an unpaired electron—making it very reactive. Nitric oxide can freely diffuse through aqueous solutions or membranes, reacting rapidly with metal centers in cellular proteins and with reactive groups in other cellular molecules.
Nitric oxide is produced in the body by an enzyme called nitric oxide synthase, which converts the amino acid L-arginine to nitric oxide and L-citrulline. There are three types of nitric oxide synthase: brain, endothelial, and inducible. Both brain and endothelial enzymes are constitutive, that is, they are always present in cells, while the production of inducible nitric oxide synthase can be turned on or off when a system needs nitric oxide. After nitric oxide is produced in specific areas of the body by nitric oxide synthase, it diffuses to nearby cells. Nitric oxide then reacts preferentially in the interior of these cells with the metal centers of proteins. Nitric oxide binds specifically to the iron (Fe) atom of the heme group in proteins; it can also interact with other metal sites in proteins as well as with the thiol group (SH) of the amino acid cysteine. The interaction of nitric oxide with these proteins causes a cascade of intracellular events that leads to specific physiological changes within cells. For example, nitric oxide causes the smooth muscle cells surrounding blood vessels to relax, decreasing blood pressure. Nitric oxide plays an important role in the central and peripheral nervous systems; the overproduction of nitric oxide in brain tissues has been implicated in stroke and other neurological problems.
Nitric oxide also functions as an important agent in the immune system by killing invading bacterial cells. Nitric oxide released by macrophages can inhibit important cellular processes in the bacteria, including deoxyribonucleic acid (DNA) synthesis and respiration, by binding to and destroying iron-sulfur centers in key enzymes in these pathways.
Although nitric oxide production in the immune system serves a crucial biological function, there can be adverse effects when too much nitric oxide is produced. During a massive bacterial infection, excess nitric oxide can go into the vascular system, causing a dramatic decrease in blood pressure, which may lead to possibly fatal septic shock. Thus, scientists are working on drugs that can selectively inhibit the inducible form of nitric oxide synthase in order to avoid the harmful effects produced by excess nitric oxide without interfering with useful nitric oxide pathways.
Oxford Companion to the Body:
nitric oxide |
Two strands of research in the late 1970s led to a revolution in biology. Robert Furchgott was unravelling a paradox concerning the well-known neurotransmitter acetylcholine: when injected intravenously it lowers blood pressure, showing that the body's blood vessels are relaxing, but when applied directly to blood vessels in isolation, outside the body, acetylcholine normally makes them contract. Furchgott showed that the response of blood vessels depended critically on the innermost layer of cells lining the vessel — the endothelium. When the endothelium was present, acetylcholine relaxed blood vessels, but when it was removed they contracted. Acetylcholine was shown to cause the release of a diffusible factor from endothelium, and it was this endothelium-derived relaxing factor (EDRF) — its nature then unknown — which relaxed the blood vessels.
Meanwhile, Ferid Murad was investigating how blood vessels are relaxed by the nitrovasodilators (e.g. glyceryl trinitrate, amyl nitrite) used in the treatment of angina. He found that these compounds increase the levels of cyclic GMP (known to promote relaxation) inside the smooth muscle cells of the vessels, probably by generating the substance nitric oxide (more correctly called nitrogen monoxide; NO).
It was soon shown that EDRF also increases the levels of cyclic GMP in smooth muscle, and the two lines of research converged when it was found that various agents, including haemoglobin and the dye methylene blue, inhibit the action both of EDRF and of the nitrovasodilators. By 1987, Furchgott and Louis Ignarro were suggesting that EDRF and NO were one and the same. This was confirmed by Salvador Moncada, who showed that NO is synthesized from the dietary amino acid L-arginine.
It then became evident that the endothelium of blood vessels was not the only site where NO is made. The enzyme nitric oxide synthase (NOS), which uses L-arginine, oxygen, and cofactors to make NO, exists in three forms: neuronal NOS (nNOS), from nerve cells; inducible NOS (iNOS), in inflammatory and other cells when the body's defence mechanisms are activated; and endothelial NOS (eNOS). nNOS and eNOS are ‘constitutive’ enzymes — that is, they are always present in their cells — and they are activated by increases in the intracellular concentration of calcium ions. iNOS is produced in many cells in response to bacterial infection and other circumstances (such as rheumatoid arthritis) when the immune system is activated; it is not regulated by calcium.
Nitric oxide is a tiny molecule. It is a gas, but dissolves in the fluids in and around cells. It is a free radical (sometimes denoted •NO to show that it has an unpaired electron, which makes it react very readily with other molecules). In particular, NO reacts with the radical anion, superoxide (•O2-), to form peroxynitrite (ONOO-), which can damage cellular DNA and hence cause cell death. Thus, excess NO can cause damage to cells. In some situations this is valuable: for instance, cells of the immune system use NO to kill invading bacteria. However, it can also be dangerous. After a stroke, for example, the nerve cells that have been deprived of oxygen fail to control their intracellular calcium; this rises and triggers a massive synthesis of NO by nNOS activation, leading to peroxynitrite production and the death of surrounding neurons. Peroxynitrite also oxidizes low density lipoproteins (LDL), which carry cholesterol in the blood, and oxidized LDL promotes atherosclerosis of blood vessels.
In septicaemia (blood poisoning), bacteria circulate in large numbers in the blood, and, in response, much NO is produced by many types of cells, including the muscle cells of the blood vessels this causes the blood vessels to relax. This leads to a severe fall in blood pressure, septic shock, which is difficult to reverse with agents such as adrenaline and dopamine, which normally increase blood pressure by constricting blood vessels. Septicaemia causes many deaths each year, and inhibition of NO synthesis appeared to be a promising treatment. But early attempts using inhibitors of NOS were largely unsuccessful. However, these were not selective for the relevant type (iNOS) and simultaneous inhibition of eNOS was deleterious to organ function. The increase in iNOS activity in inflammation can be inhibited by glucocorticoids (e.g. prednisolone, corticosterone), which explains part of their anti-inflammatory action, but they have no effect on the level of enzyme once it has been made. Thus the search is on for selective iNOS inhibitors which will leave nNOS and eNOS uninhibited.
NO has a good side and a bad side. While excess NO in septicaemia, inflammation, and stroke causes severe damage, localized production of small quantities of NO is essential for normal body function. Endothelial NOS maintains blood vessel function, and inhibition of this enzyme increases blood pressure. Indeed, hypertension is associated with decreased effectiveness of endothelial NO mechanisms. In blood vessels NO also regulates multiplication of muscle cells. Coronary artery bypass surgery sometimes fails because of narrowing of the newly replaced vessels; this is caused by thickening of their walls through muscle cell proliferation — thought to be due to decreased local production of NO as a result of endothelial damage during the surgery.
NO acts as a neurotransmitter in nerves involved in controlling a number of ‘vegetative’ functions, including operation of the sphincters in the gut and erection of the penis. Viagra (Sildenafil) works by prolonging the actions of NO released from penile nerves. In the brain, NO could even be involved in the formation of memory. ‘Long-term potentiation’ — the increase in strength of synapses in the hippocampus, as a result of strong stimulation which is thought to underlie certain forms of memory — is blocked by drugs that inhibit NO synthesis.
This small inorganic molecule, which was probably best known to the general public as a pollutant in car exhausts, became the biological molecule of the 1990s. Its importance was recognized by the award of a Nobel Prize to Furchgott, Ignarro, and Murad in 1998 ‘for their discoveries concerning nitric oxide as a signalling molecule in the cardiovascular system’.
— C. Robin Hiley
See also blood vessels.
Drug Info:
Nitric Oxide |
Brand names: INOmax®
Chemical formula:
Nitric Oxide inhalation gas
What is nitric oxide inhalation gas?
NITRIC OXIDE (INOmax™) is a drug that relaxes blood vessels in the lungs. It decreases blood pressure in the lungs and helps them to work better. Generic nitric oxide inhalation gas is not available.
What should I tell my health care provider before I take this medicine?
They need to know if you have any of these conditions:
• bleeding problems
• heart defect
• heart failure
• low platelet counts
• lung infection or chronic lung disease
• methemoglobin reductase deficiency
• an unusual or allergic reaction to nitric oxide, other medicines, foods, dyes, or preservatives
• pregnant or trying to get pregnant
• breast-feeding
How should I use this medicine?
Nitric oxide is breathed in while you are on a breathing machine. It is given by a trained health care professional in a hospital setting.
What drug(s) may interact with nitric oxide?
• monoamine oxidase inhibitors (Azilect®, Eldepryl®, Emsam®, Marplan®, Nardil®, Parnate®, Zelapar™)
• nitroglycerin
• nitroprusside
Tell your prescriber or health care professional about all other medicines that you are taking, including non-prescription medicines, nutritional supplements, or herbal products. Also tell your prescriber or health care professional if you are a frequent user of drinks with caffeine or alcohol, if you smoke, or if you use illegal drugs. These may affect the way your medicine works. Check with your health care professional before stopping or starting any of your medicines.
What should I watch for while taking nitric oxide?
Your condition will be closely monitored while you receive nitric oxide.
What side effects may I notice from receiving nitric oxide?
Side effects that you should report to your prescriber or health care professional as soon as possible:
• blood in the urine
• high blood sugar
• increased difficulty breathing
• infection
• low blood pressure
• skin infection
Where can I keep my medicine?
This does not apply. Inhaled nitric oxide is only given in a hospital setting.
Last updated: 7/1/2002
Important Disclaimer: The drug information provided here is for educational purposes only. It is intended to supplement, not substitute for, the diagnosis, treatment and advice of a medical professional. This drug information does not cover all possible uses, precautions, side effects and interactions. It should not be construed to indicate that this or any drug is safe for you. Consult your medical professional for guidance before using any prescription or over the counter drugs.
Oxford Dictionary of Sports Science & Medicine:
nitric oxide |
A compound released during exercise by the action of an enzyme, nitric oxide synthase, in cells lining arteries. Nitric oxide causes the arteries to dilate and prolongs vasodilation, thereby facilitating blood flow to muscle cells. Nitric oxide is used to treat people with obstructive pulmonary disease. Purveyors of dietary supplements containing substances (e.g. L-arginine) that increase nitric oxide levels in the blood, claim that the supplements enhance athletic performance by enabling nutritionally rich blood to flow more easily to skeletal muscles. Sometimes these supplements are marketed as ‘haemodilators’. Scientific studies carried out in 2004 indicate that nitric oxide supplements have no significant ergogenic effect on healthy individuals, and taking large doses of supplements could be dangerous to health.
Columbia Encyclopedia:
nitric oxide |
In the environment, nitric oxide is a precursor of smog and acid rain. Nitric oxide in minute amounts serves as a source of energy in certain bacteria. In the body, it serves as a chemical messenger with a wide range of functions. It acts as a neurotransmitter and is necessary for penile erection. It affects blood pressure and is produced by macrophages in the immune system to help defend against infection and cancer. Despite its usefulness, nitric oxide can have a toxic effect on body cells and has been implicated in Huntington's disease and Alzheimer's disease.
Oxford Dictionary of Biochemistry:
nitric oxide |
| nitrene, nitrate reduction, nitrate reductase | |
| nitric-oxide synthase, nitrification, nitrify |
Wikipedia on Answers.com:
Nitric oxide |
| Nitric oxide | |
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Nitric oxide |
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Oxidonitrogen(•)[1] (additive) |
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Other names
Nitrogen monoxide |
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| Identifiers | |
| CAS number | 10102-43-9  |
| PubChem | 145068 |
| ChemSpider | 127983 |
| UNII | 31C4KY9ESH |
| EC number | 233-271-0 |
| UN number | 1660 |
| DrugBank | DB00435 |
| KEGG | D00074 |
| ChEBI | CHEBI:16480 |
| ChEMBL | CHEMBL1200689  |
| RTECS number | QX0525000 |
| ATC code | R07 |
| Gmelin Reference | 451 |
| 3DMet | B00122 |
| Jmol-3D images | Image 1 |
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| Properties | |
| Molecular formula | NO |
| Molar mass | 30.01 g mol−1 |
| Exact mass | 29.997988627 g mol−1 |
| Appearance | Colourless gas |
| Density | 1.3402 g dm−3 |
| Melting point |
−164 °C, 109 K, -263 °F |
| Boiling point |
−152 °C, 121 K, -242 °F |
| Solubility in water | 74 cm3 dm−3 |
| Refractive index (nD) | 1.0002697 |
| Structure | |
| Molecular shape | linear (point group C∞v) |
| Thermochemistry | |
| Std enthalpy of formation ΔfH |
90.29 kJ mol−1 |
| Standard molar entropy S |
210.76 J K−1 mol−1 |
| Pharmacology | |
| Bioavailability | good |
| Routes of administration |
Inhalation |
| Metabolism | via pulmonary capillary bed |
| Elimination half-life |
2–6 seconds |
| Hazards | |
| MSDS | External MSDS |
| EU classification |  O  T |
| R-phrases | R8, R23, R34, R44 |
| S-phrases | (S1), S17, S23, S36/37/39, S45 |
| NFPA 704 |
 0
3
3
OX
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| Related compounds | |
| Related nitrogen oxides | Dinitrogen pentoxide Dinitrogen tetroxide |
 (verify) (what is:  / ?)Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
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| Infobox references | |
Nitric oxide, also known as nitrogen monoxide, is a binary molecule with chemical formula NO. It is a free radical[2] and is an important intermediate in the chemical industry. Nitric oxide is a by-product of combustion of substances in the air, as in automobile engines, fossil fuel power plants, and is produced naturally during the electrical discharges of lightning in thunderstorms.
In mammals including humans, NO is an important cellular signaling molecule involved in many physiological and pathological processes.[3] It is a powerful vasodilator with a short half-life of a few seconds in the blood. Long-known pharmaceuticals like nitroglycerine and amyl nitrite were discovered, more than century after their first use in medicine, to be active through the mechanism of being precursors to nitric oxide.
Low levels of nitric oxide production are important in protecting organs such as the liver from ischemic damage. Chronic expression of NO is associated with various carcinomas and inflammatory conditions including Type-1 diabetes, multiple sclerosis, arthritis and ulcerative colitis.[citation needed]
Nitric oxide should not be confused with nitrous oxide (N2O), an anaesthetic and greenhouse gas, or with nitrogen dioxide (NO2), a brown toxic gas and a major air pollutant. However, nitric oxide is rapidly oxidised in air to nitrogen dioxide. Humphrey Davy discovered this to his discomfort, when he inhaled the gas early in his career.
Despite being a simple molecule, NO is an important biological regulator and is a fundamental component in the fields of neuroscience, physiology, and immunology, with discovery of its key roles leading to Nobel Prize winning research in these areas. It was proclaimed “Molecule of the Year” in 1992.[4]
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Contents
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Commercially, NO is produced by the oxidation of ammonia at 750 °C to 900 °C (normally at 850 °C) with platinum as catalyst:
The uncatalyzed endothermic reaction of O2 and N2, which is performed at high temperature (>2000 °C) by lightning has not been developed into a practical commercial synthesis (see Birkeland–Eyde process):
In the laboratory, nitric oxide is conveniently generated by reduction of nitric acid with copper:
or by the reduction of nitrous acid in the form of sodium nitrite or potassium nitrite:
The iron(II) sulfate route is simple and has been used in undergraduate laboratory experiments.
So-called NONOate compounds are also used for NO generation.
NO reacts with all transition metals to give complexes called metal nitrosyls. The most common bonding mode of NO is the terminal linear type (M-NO). The angle of the M-N-O group varies from 160° to 180° but is still termed "linear". In this case, the NO group is considered a 3-electron donor under the covalent (neutral) method of electron counting, or a 2-electron donor under the ionic method.[7] In the case of a bent M-N-O conformation, the NO group can be considered a one-electron donor using neutral counting, or a 2-electron donor using ionic counting.[8] One can view such complexes as derived from NO+, which is isoelectronic with CO.
Nitric oxide can serve as a one-electron pseudohalide. In such complexes, the M-N-O group is characterized by an angle between 120° and 140°.
The NO group can also bridge between metal centers through the nitrogen atom in a variety of geometries.
_(white)_in_the_cytoplasm_(green)_of_clusters_of_conifer_cells_one_hour_after_mechanical_agitation.jpg)
Nitric oxide concentration can be determined using a simple chemiluminescent reaction involving ozone:[9] A sample containing nitric oxide is mixed with a large quantity of ozone. The nitric oxide reacts with the ozone to produce oxygen and nitrogen dioxide. This reaction also produces light (chemiluminescence), which can be measured with a photodetector. The amount of light produced is proportional to the amount of nitric oxide in the sample.
Other methods of testing include electroanalysis (amperometric approach), where NO reacts with an electrode to induce a current or voltage change. The detection of NO radicals in biological tissues is particularly difficult due to the short lifetime and concentration of these radicals in tissues. One of the few practical methods is spin trapping of nitric oxide with iron-dithiocarbamate complexes and subsequent detection of the mono-nitrosyl-iron complex with electron paramagnetic resonance (EPR).[10][11]
A group of fluorescent dye indicators that are also available in acetylated form for intracellular measurements exist. The most common compound is 4,5-diaminofluorescein (DAF-2).[4]
From a thermodynamic perspective, NO is unstable with respect to O2 and N2, although this conversion is very slow at ambient temperatures in the absence of a catalyst. Because the heat of formation of NO is endothermic, its synthesis from molecular nitrogen and oxygen requires elevated temperatures above 1000 °C. A major natural source is lightning. The use of internal combustion engines has drastically increased the presence of nitric oxide in the environment. One purpose of catalytic converters in cars is to minimize NO emission by catalytic reversion to O2 and N2.
Nitric oxide in the air may convert to nitric acid, which has been implicated in acid rain. However, it is an important source of nutrition for plant life in the form of nitrates. Furthermore, both NO and NO2 participate in ozone layer depletion. Nitric oxide is a small highly diffusible gas and a ubiquitous bioactive molecule.
Although NO has relatively few direct uses, it is produced on a massive scale as an intermediate in the Ostwald process for the synthesis of nitric acid from ammonia. In 2005, the US alone produced 6 million metric tons of nitric acid.[12] It finds use in the semiconductor industry for various processes. In one of its applications it is used along with nitrous oxide to form oxynitride gates in CMOS devices.
Nitric oxide can be used for detecting surface radicals on polymers. Quenching of surface radicals with nitric oxide results in incorporation of nitrogen, which can be quantified by means of X-ray photoelectron spectroscopy.
NO is one of the few gaseous signaling molecules known and is additionally exceptional due to the fact that it is a radical gas. It is a key vertebrate biological messenger, playing a role in a variety of biological processes. It is a known bioproduct in almost all type of organisms, ranging from bacteria to plants, fungi and animal cells[13]. Nitric oxide, known as the 'endothelium-derived relaxing factor', or 'EDRF', is biosynthesized endogenously from L-arginine, oxygen and NADPH by various nitric oxide synthase (NOS) enzymes. Reduction of inorganic nitrate may also serve to make nitric oxide. The endothelium (inner lining) of blood vessels uses nitric oxide to signal the surrounding smooth muscle to relax, thus resulting in vasodilation and increasing blood flow. Nitric oxide is highly reactive (having a lifetime of a few seconds), yet diffuses freely across membranes. These attributes make nitric oxide ideal for a transient paracrine (between adjacent cells) and autocrine (within a single cell) signaling molecule.[14] The production of nitric oxide is elevated in populations living at high altitudes, which helps these people avoid hypoxia by aiding in pulmonary vasculature vasodilation. Effects include vasodilatation, neurotransmission (see gasotransmitters), modulation of the hair cycle,[15] production of reactive nitrogen intermediates and penile erections (through its ability to vasodilate). Nitroglycerin and amyl nitrite serve as vasodilators because they are converted to nitric oxide in the body. The vasodialating antihypertensive drug minoxidil contains an NO moity and may act as an NO agonist. Similarly, Sildenafil citrate, popularly known by the trade name Viagra, stimulates erections primarily by enhancing signaling through the nitric oxide pathway in the penis.
Nitric oxide (NO) contributes to vessel homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium. Humans with atherosclerosis, diabetes, or hypertension often show impaired NO pathways.[16] A high salt intake was demonstrated to attenuate NO production in patients with essential hypertension, although bioavailability remains unregulated.[17]
Nitric oxide is also generated by phagocytes (monocytes, macrophages, and neutrophils) as part of the human immune response. Phagocytes are armed with inducible nitric oxide synthase (iNOS), which is activated by interferon-gamma (IFN-γ) as a single signal or by tumor necrosis factor (TNF) along with a second signal.[18] On the other hand, transforming growth factor-beta (TGF-β) provides a strong inhibitory signal to iNOS, whereas interleukin-4 (IL-4) and IL-10 provide weak inhibitory signals. In this way the immune system may regulate the armamentarium of phagocytes that play a role in inflammation and immune responses. Nitric oxide secreted as an immune response is as free radicals and is toxic to bacteria; the mechanism for this includes DNA damage[19][20][21] and degradation of iron sulfur centers into iron ions and iron-nitrosyl compounds.[22] In response, however, many bacterial pathogens have evolved mechanisms for nitric oxide resistance.[23] Because nitric oxide might serve as an inflammometer in conditions like asthma, there has been increasing interest in the use of exhaled nitric oxide as a breath test in diseases with airway inflammation. Reduced levels of exhaled NO have been associated with exposure to air pollution.[24]
Nitric oxide can contribute to reperfusion injury when an excessive amount produced during reperfusion (following a period of ischemia) reacts with superoxide to produce the damaging oxidant peroxynitrite. In contrast, inhaled nitric oxide has been shown to help survival and recovery from paraquat poisoning, which produces lung tissue–damaging superoxide and hinders NOS metabolism.
In plants, nitric oxide can be produced by any of four routes: (i) L-arginine-dependent nitric oxide synthase,[25][26][27] (although the existence of animal NOS homologs in plants is debated),[28] (ii) by plasma membrane-bound nitrate reductase, (iii) by mitochondrial electron transport chain, or (iv) by non-enzymatic reactions. It is a signaling molecule, acts mainly against oxidative stress and also plays a role in plant pathogen interactions. Treating cut flowers and other plants with nitric oxide has been shown to lengthen the time before wilting.[29]
An important biological reaction of nitric oxide is S-nitrosylation, the conversion of thiol groups, including cysteine residues in proteins, to form S-nitrosothiols (RSNOs). S-Nitrosylation is a mechanism for dynamic, post-translational regulation of most or all major classes of protein.
There are several mechanisms by which NO has been demonstrated to affect the biology of living cells. These include oxidation of iron-containing proteins such as ribonucleotide reductase and aconitase, activation of the soluble guanylate cyclase, ADP ribosylation of proteins, protein sulfhydryl group nitrosylation, and iron regulatory factor activation.[30] NO has been demonstrated to activate NF-κB in peripheral blood mononuclear cells, an important transcription factor in iNOS gene expression in response to inflammation.[31] It was found that NO acts through the stimulation of the soluble guanylate cyclase, which is a heterodimeric enzyme with subsequent formation of cyclic GMP. Cyclic GMP activates protein kinase G, which causes phosphorylation of myosin light chain phosphatase, and therefore inactivation of myosin light-chain kinase, and leads ultimately to the dephosphorylation of the myosin light chain, causing smooth muscle relaxation.[32]
Nitric oxide/oxygen blends are used in critical care to promote capillary and pulmonary dilation to treat primary pulmonary hypertension in neonatal patients[33][34] post-meconium aspiration and related to birth defects. These are often a last-resort gas mixture before the use of extracorporeal membrane oxygenation (ECMO). Nitric oxide therapy has the potential to significantly increase the quality of life and, in some cases, save the lives of infants at risk for pulmonary vascular disease.[35]
Nitric oxide is also administered as salvage therapy in patients with acute right ventricular failure secondary to pulmonary embolism.[36]
Nitric oxide is considered an antianginal drug: it causes vasodilation, which can help with ischemic pain, known as angina, by decreasing the cardiac workload. By dilating (expanding) the veins, nitric oxide drugs lower arterial pressure and left ventricular filling pressure.[37] This vasodilation does not decrease the volume of blood the heart pumps, but rather it decreases the force the heart muscle must exert to pump the same volume of blood. Nitroglycerin pills, taken sublingually (under the tongue), are used to prevent or treat acute chest pain. The nitroglycerin reacts with a sulfhydryl group (–SH) to produce nitric oxide, which eases the pain by causing vasodilation. Recent evidence suggests that nitrates may be beneficial for treatment of angina due to reduced myocardial oxygen consumption both by decreasing preload and afterload and by some direct vasodilation of coronary vessels.[37]
Mainly for its utility as a vasodilator, NO has entered the fitness industry as an array of supplements geared towards accelerated muscle growth and prolonged stamina during endurance activities.[citation needed]
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
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 | American Heritage Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved. Read more |
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| Britannica Concise Encyclopedia. Britannica Concise Encyclopedia. © 1994-2012 Encyclopædia Britannica, Inc. All rights reserved. Read more |
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| McGraw-Hill Science & Technology Encyclopedia. McGraw-Hill Encyclopedia of Science and Technology. Copyright © 2005 by The McGraw-Hill Companies, Inc. All rights reserved. Read more |
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| Oxford Companion to the Body. The Oxford Companion to the Body. Copyright © 2001, 2003 by Oxford University Press. All rights reserved. Read more |
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| Drug Info. Gold Standard. Copyright © 2008 by Gold Standard. All rights reserved. Read more |
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| Oxford Dictionary of Sports Science & Medicine. The Oxford Dictionary of Sports Science & Medicine. Copyright © Michael Kent 1998, 2006, 2007. All rights reserved. Read more |
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| Columbia Encyclopedia. The Columbia Electronic Encyclopedia, Sixth Edition Copyright © 2012, Columbia University Press. Licensed from Columbia University Press. All rights reserved. www.cc.columbia.edu/cu/cup/. Read more |
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Oxford Dictionary of Biochemistry. Oxford University Press. Oxford Dictionary of Biochemistry and Molecular Biology © 1997, 2000, 2006 All rights reserved. Read more | |
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| Wikipedia on Answers.com. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article Nitric oxide. Read more |
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