A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6)
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
"Esters are organic compounds that result from the reaction between an alcohol and a carboxylic acid, playing significant roles in various biological processes and often used in pharmaceutical synthesis."
An essential amino acid that is physiologically active in the L-form.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.
Arginine derivative which is a substrate for many proteolytic enzymes. As a substrate for the esterase from the first component of complement, it inhibits the action of C(l) on C(4).
Fractionation of a vaporized sample as a consequence of partition between a mobile gaseous phase and a stationary phase held in a column. Two types are gas-solid chromatography, where the fixed phase is a solid, and gas-liquid, in which the stationary phase is a nonvolatile liquid supported on an inert solid matrix.
The methyl homolog of parathion. An effective, but highly toxic, organothiophosphate insecticide and cholinesterase inhibitor.
Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
A microanalytical technique combining mass spectrometry and gas chromatography for the qualitative as well as quantitative determinations of compounds.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
The rate dynamics in chemical or physical systems.
An alkylating agent in cancer therapy that may also act as a mutagen by interfering with and causing damage to DNA.
Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
Drugs used to cause dilation of the blood vessels.
Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)
A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)

Relaxin is a potent renal vasodilator in conscious rats. (1/3789)

The kidneys and other nonreproductive organs vasodilate during early gestation; however, the "pregnancy hormones" responsible for the profound vasodilation of the renal circulation during pregnancy are unknown. We hypothesized that the ovarian hormone relaxin (RLX) contributes. Therefore, we tested whether the administration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats. After several days of treatment with either purified porcine RLX or recombinant human RLX 2 (rhRLX), effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increased by 20%-40%. Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats, suggesting that estrogen and progesterone are unnecessary for the renal response to rhRLX. The nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester completely abrogated the increase in ERPF and GFR elicited by chronic administration of purified porcine RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcine RLX to conscious rats over several hours failed to increase ERPF and GFR. Plasma osmolality was consistently reduced by the chronic administration of both RLX preparations. In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality.  (+info)

Effects of chronic nitric oxide activation or inhibition on early hepatic fibrosis in rats with bile duct ligation. (2/3789)

Hepatic fibrosis or increased liver collagen contents drive functional abnormalities that, when extensive, may be life threatening. The purpose of this study was to assess the effects of the chronic stimulation or inhibition of nitric oxide synthesis in rats with hepatic fibrosis induced by permanent common bile duct ligation (3 weeks) and the role of expression of the different nitric oxide synthase isoforms. Bile duct ligation led to an important accumulation of collagen in the hepatic parenchyma, as shown both histologically and by the hydroxyproline contents of livers. Bilirubin and serum enzyme activities (measured as markers of cholestasis) increased several-fold after bile duct ligation. The area of fibrotic tissue, liver hydroxyproline content and serum markers of cholestasis were clearly related in obstructed rats. The absence of modifications in haemodynamic parameters excludes circulatory changes from being responsible for the development of liver alterations. In animals treated with NG-nitro-L-arginine methyl ester (L-NAME) the area of fibrosis was similar to that of untreated animals, the signs of cholestasis and cellular injury being more evident. In rats treated with L-arginine the area of fibrosis was almost three times larger than that found in bile duct ligated rats and in L-NAME-treated bile duct ligated rats, although the observed biochemical changes were similar to those seen in rats treated with L-NAME. Our results with inducible nitric oxide synthase, obtained by Western blots and immunohistochemistry, indicate a greater expression of the inducible enzyme in bile duct ligated and L-arginine-treated animals and a lower expression in the L-NAME and control groups. Constitutive nitric oxide synthase expression, obtained by Western blots, was very similar in all groups, except for the L-arginine-treated rats in which it was lower. These results suggest that nitric oxide production may be a key factor in the development of fibrosis in bile duct ligated rats. They also support the hypothesis of a dual role for nitric oxide; one beneficial, mediated by its circulatory effects, and the second negative, through its local toxic effects.  (+info)

Impairment of neocortical long-term potentiation in mice deficient of endothelial nitric oxide synthase. (3/3789)

The role of the possible retrograde messenger nitric oxide (NO) in the induction of long-term potentiation (LTP) was studied in supragranular layers of somatosensory cortical slices obtained from adult mice. High-frequency stimulation produced a slowly rising, long-lasting (50 min) and significant (P < 0.001) increase in the extracellular synaptic response by 23%. The induction of LTP was independent from activation of N-methyl-D-aspartate (NMDA) receptors, but prevented by bath application of NG-nitro-L-arginine methyl ester (L-NAME), indicating that one or several of the different NO synthases (NOS) produced NO within the postsynaptic neuron. No LTP could be induced in knockout mice lacking the endothelial NOS (eNOS) isoform. These data suggest that eNOS is involved in an NMDA receptor-independent form of LTP in the rodent cerebral cortex.  (+info)

L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide. (4/3789)

The mechanism of L-arginine stimulation of glucose-induced insulin secretion from mouse pancreatic islets was studied. At 16.7 mmol/l glucose, L-arginine (10 mmol/l) potentiated both phases 1 and 2 of glucose-induced insulin secretion. This potentiation of glucose-induced insulin secretion was mimicked by the membrane depolarizing agents tetraethylammonium (TEA, 20 mmol/l) and K+ (60 mmol/l), which at 16.7 mmol/l glucose obliterated L-arginine (10 mmol/l) modulation of insulin secretion. Thus L-arginine may potentiate glucose-induced insulin secretion by stimulation of membrane depolarization. At 3.3 mmol/l glucose, L-arginine (10 mmol/l) failed to stimulate insulin secretion. In accordance with membrane depolarization by the electrogenic transport of L-arginine, however, L-arginine (10 mmol/l) stimulation of insulin secretion was enabled by the K+ channel inhibitor TEA (20 mmol/l), which potentiates membrane depolarization by L-arginine. Furthermore, L-arginine (10 mmol/l) stimulation of insulin secretion was permitted by forskolin (10 micromol/l) or tetradecanoylphorbol 13-acetate (0.16 micromol/l), which, by activation of protein kinases A and C respectively sensitize the exocytotic machinery to L-arginine-induced Ca2+ influx. Thus glucose may sensitize L-arginine stimulation of insulin secretion by potentiation of membrane depolarization and by activation of protein kinase A or protein kinase C. Finally, L-arginine stimulation of glucose-induced insulin secretion was mimicked by NG-nitro-L-arginine methyl ester (10 mmol/l), which stimulates membrane depolarization but inhibits nitric oxide synthase, suggesting that L-arginine-derived nitric oxide neither inhibits nor stimulates insulin secretion. In conclusion, it is suggested that L-arginine potentiation of glucose-induced insulin secretion occurs independently of nitric oxide, but is mediated by membrane depolarization, which stimulates insulin secretion through protein kinase A- and C-sensitive mechanisms.  (+info)

Influence of nitric oxide modulators on cholinergically stimulated hormone release from mouse islets. (5/3789)

1. We have investigated, with a combined in vitro and in vivo approach, the influence on insulin and glucagon release stimulated by the cholinergic, muscarinic agonist carbachol of different NO modulators, i.e. the nitric oxide synthase (NOS) inhibitors NG-nitro-L-arginine methyl ester (L-NAME), NG-monomethyl-L-arginine (L-NMMA) and 7-nitroindazole as well as the intracellular NO donor hydroxylamine. 2. At basal glucose (7 mM) carbachol dose-dependently stimulated insulin release from isolated islets with a half-maximal response at approximately 1 microM of the agonist. In the presence of 5 mM L-NAME (a concentration that did not influence basal insulin release) the insulin response was markedly increased along the whole dose-response curve and the threshold for carbachol stimulation was significantly lowered. 3. Carbachol-stimulated islets displayed an increased insulin release and a suppressed glucagon release in the presence of L-NAME, L-NMMA or 7-nitroindazole. Significant suppression of glucagon release (except for L-NAME) was achieved at lower concentrations (approximately 0.1-0.5 mM) of the NOS inhibitors than the potentiation of insulin release (1.0-5.0 mM). The intracellular NO donor hydroxylamine dose-dependently inhibited carbachol-induced insulin release but stimulated glucagon release only at a low concentration (3 microM). 4. In islets depolarized with 30 mM K+ in the presence of the KATP channel opener diazoxide, NOS inhibition by 5 mM L-NAME still markedly potentiated carbachol-induced insulin release (although less so than in normal islets) and suppressed glucagon release. 5. In vivo pretreatment of mice with L-NAME was followed by a markedly increased insulin release and a reduced glucagon release in response to an i.v. injection of carbachol. 6. The data suggest that NO is a negative modulator of insulin release but a positive modulator of glucagon release induced by cholinergic muscarinic stimulation. These effects were also evident in K+ depolarized islets and thus NO might exert a major influence on islet hormone secretion independently of membrane depolarization events.  (+info)

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig. (6/3789)

1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated.  (+info)

Role of iNOS in the vasodilator responses induced by L-arginine in the middle cerebral artery from normotensive and hypertensive rats. (7/3789)

1. The substrate of nitric oxide synthase (NOS), L-arginine (L-Arg, 0.01 microM - 1 mM), induced endothelium-independent relaxations in segments of middle cerebral arteries (MCAs) from normotensive Wistar-Kyoto (WKY) and hypertensive rats (SHR) precontracted with prostaglandin F2alpha (PGF2alpha). These relaxations were higher in SHR than WKY arteries. 2. L-N(G)-nitroarginine methyl ester (L-NAME) and 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), unspecific and inducible NOS (iNOS) inhibitors, respectively, reduced those relaxations, specially in SHR. 3. Four- and seven-hours incubation with dexamethasone reduced the relaxations in MCAs from WKY and SHR, respectively. 4. Polymyxin B and calphostin C, protein kinase C (PKC) inhibitors, reduced the L-Arg-induced relaxation. 5. Lipopolysaccharide (LPS, 7 h incubation) unaltered and inhibited these relaxations in WKY and SHR segments, respectively. LPS antagonized the effect polymyxin B in WKY and potentiated L-Arg-induced relaxations in SHR in the presence of polymyxin B. 6. The contraction induced by PGF2alpha was greater in SHR than WKY arteries. This contraction was potentiated by dexamethasone and polymyxin B although the effect of polymyxin B was higher in SHR segments. LPS reduced that contraction and antagonized dexamethasone- and polymyxin B-induced potentiation, these effects being greater in arteries from SHR. 7. These results suggest that in MCAs: (1) the induction of iNOS participates in the L-Arg relaxation and modulates the contraction to PGF2alpha; (2) that induction is partially mediated by a PKC-dependent mechanism; and (3) the involvement of iNOS in such responses is greater in the hypertensive strain.  (+info)

Effect of acute and long-term treatment with 17-beta-estradiol on the vasomotor responses in the rat aorta. (8/3789)

1. This study sought to evaluate whether the effects of acute and long-term treatment with 17-beta-estradiol on the vasomotor responses in rat aortic rings are mediated through the same mechanism. 2. Ovariectomized rats were treated daily with either 17-beta-estradiol-3-benzoate (100 microg kg(-1)) or vehicle for 1 week. 3. The effect of long-term 17-beta-estradiol treatment on the responses to cumulative doses of phenylephrine, 5-HT, calcium, potassium and 17-beta-estradiol was determined in aortic rings. In the same rings, the effect of acute exposure to 17-beta-estradiol (5 and 10 microM) on the dose response curves for phenylephrine, 5-HT, calcium, potassium and acetylcholine were estimated. The measurements were made in rings with and without intact endothelium. The tone-related basal release of nitric oxide (NO) was measured in rings with intact endothelium. 4. Long-term 17-beta-estradiol treatment reduced the maximum developed contraction to all contracting agents studied. This effect was abolished in endothelium denuded vessels. Acute 17-beta-estradiol treatment also reduced maximal contraction. This effect, however, was independent of the endothelium. 5. Long-term 17-beta-estradiol treatment significantly increased the ability of the rings to dilate in response to acetylcholine whereas acute exposure to 17-beta-estradiol had no effect. The tone-related release of NO was significantly increased after long-term exposure to 17-beta-estradiol. 6. In conclusion, this study indicate that the acute and long-term effects of 17-beta-estradiol in the rat aorta are mediated through different mechanisms. The long-term effect is mediated through the endothelium most likely by increasing NO release. In contrast, the acute effect of 17-beta-estradiol seems to be through an effect on the vascular smooth muscle cells.  (+info)

NG-Nitroarginine Methyl Ester (L-NAME) is not a medication, but rather a research chemical used in scientific studies. It is an inhibitor of nitric oxide synthase, an enzyme that synthesizes nitric oxide, a molecule involved in the relaxation of blood vessels.

Therefore, L-NAME is often used in experiments to investigate the role of nitric oxide in various physiological and pathophysiological processes. It is important to note that the use of L-NAME in humans is not approved for therapeutic purposes due to its potential side effects, which can include hypertension, decreased renal function, and decreased cerebral blood flow.

Nitro-L-arginine or Nitroarginine is not a medical term per se, but it is a chemical compound that is sometimes used in medical research and experiments. It is a salt of nitric acid and L-arginine, an amino acid that is important for the functioning of the body.

Nitroarginine is known to inhibit the production of nitric oxide, a molecule that plays a role in various physiological processes such as blood flow regulation, immune response, and neurotransmission. As a result, nitroarginine has been used in research to study the effects of reduced nitric oxide levels on different systems in the body.

It's worth noting that nitroarginine is not approved for use as a medication in humans, and its use is generally limited to laboratory settings.

Nitric Oxide Synthase (NOS) is a group of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. There are three distinct isoforms of NOS, each with different expression patterns and functions:

1. Neuronal Nitric Oxide Synthase (nNOS or NOS1): This isoform is primarily expressed in the nervous system and plays a role in neurotransmission, synaptic plasticity, and learning and memory processes.
2. Inducible Nitric Oxide Synthase (iNOS or NOS2): This isoform is induced by various stimuli such as cytokines, lipopolysaccharides, and hypoxia in a variety of cells including immune cells, endothelial cells, and smooth muscle cells. iNOS produces large amounts of NO, which functions as a potent effector molecule in the immune response, particularly in the defense against microbial pathogens.
3. Endothelial Nitric Oxide Synthase (eNOS or NOS3): This isoform is constitutively expressed in endothelial cells and produces low levels of NO that play a crucial role in maintaining vascular homeostasis by regulating vasodilation, inhibiting platelet aggregation, and preventing smooth muscle cell proliferation.

Overall, NOS plays an essential role in various physiological processes, including neurotransmission, immune response, cardiovascular function, and respiratory regulation. Dysregulation of NOS activity has been implicated in several pathological conditions such as hypertension, atherosclerosis, neurodegenerative diseases, and inflammatory disorders.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

Esters are organic compounds that are formed by the reaction between an alcohol and a carboxylic acid. They are widely found in nature and are used in various industries, including the production of perfumes, flavors, and pharmaceuticals. In the context of medical definitions, esters may be mentioned in relation to their use as excipients in medications or in discussions of organic chemistry and biochemistry. Esters can also be found in various natural substances such as fats and oils, which are triesters of glycerol and fatty acids.

Arginine is an α-amino acid that is classified as a semi-essential or conditionally essential amino acid, depending on the developmental stage and health status of the individual. The adult human body can normally synthesize sufficient amounts of arginine to meet its needs, but there are certain circumstances, such as periods of rapid growth or injury, where the dietary intake of arginine may become necessary.

The chemical formula for arginine is C6H14N4O2. It has a molecular weight of 174.20 g/mol and a pKa value of 12.48. Arginine is a basic amino acid, which means that it contains a side chain with a positive charge at physiological pH levels. The side chain of arginine is composed of a guanidino group, which is a functional group consisting of a nitrogen atom bonded to three methyl groups.

In the body, arginine plays several important roles. It is a precursor for the synthesis of nitric oxide, a molecule that helps regulate blood flow and immune function. Arginine is also involved in the detoxification of ammonia, a waste product produced by the breakdown of proteins. Additionally, arginine can be converted into other amino acids, such as ornithine and citrulline, which are involved in various metabolic processes.

Foods that are good sources of arginine include meat, poultry, fish, dairy products, nuts, seeds, and legumes. Arginine supplements are available and may be used for a variety of purposes, such as improving exercise performance, enhancing wound healing, and boosting immune function. However, it is important to consult with a healthcare provider before taking arginine supplements, as they can interact with certain medications and have potential side effects.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Vasodilation is the widening or increase in diameter of blood vessels, particularly the involuntary relaxation of the smooth muscle in the tunica media (middle layer) of the arteriole walls. This results in an increase in blood flow and a decrease in vascular resistance. Vasodilation can occur due to various physiological and pathophysiological stimuli, such as local metabolic demands, neural signals, or pharmacological agents. It plays a crucial role in regulating blood pressure, tissue perfusion, and thermoregulation.

Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.

In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.

In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.

Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

Cholesteryl esters are formed when cholesterol, a type of lipid (fat) that is important for the normal functioning of the body, becomes combined with fatty acids through a process called esterification. This results in a compound that is more hydrophobic (water-repelling) than cholesterol itself, which allows it to be stored more efficiently in the body.

Cholesteryl esters are found naturally in foods such as animal fats and oils, and they are also produced by the liver and other cells in the body. They play an important role in the structure and function of cell membranes, and they are also precursors to the synthesis of steroid hormones, bile acids, and vitamin D.

However, high levels of cholesteryl esters in the blood can contribute to the development of atherosclerosis, a condition characterized by the buildup of plaque in the arteries, which can increase the risk of heart disease and stroke. Cholesteryl esters are typically measured as part of a lipid profile, along with other markers such as total cholesterol, HDL cholesterol, and triglycerides.

Tosylarginine Methyl Ester (TAME) is not a medication or a therapeutic agent, but it is a research compound used in scientific studies. It is a synthetic molecule that is often used as a control or a reference standard in enzyme inhibition assays. TAME is an esterified form of the amino acid arginine, with a tosyl group (p-toluenesulfonyl) attached to the nitrogen atom.

TAME is specifically used as a selective and reversible inhibitor of the enzyme called butyrylcholinesterase (BChE), which is involved in the breakdown of certain neurotransmitters in the body. By inhibiting BChE, TAME can help to increase the levels of these neurotransmitters in the brain, making it a useful tool for studying the mechanisms of this enzyme and its role in various physiological processes.

It's important to note that while TAME is used in research settings, it is not approved for use as a drug or therapeutic agent in humans or animals.

Chromatography, gas (GC) is a type of chromatographic technique used to separate, identify, and analyze volatile compounds or vapors. In this method, the sample mixture is vaporized and carried through a column packed with a stationary phase by an inert gas (carrier gas). The components of the mixture get separated based on their partitioning between the mobile and stationary phases due to differences in their adsorption/desorption rates or solubility.

The separated components elute at different times, depending on their interaction with the stationary phase, which can be detected and quantified by various detection systems like flame ionization detector (FID), thermal conductivity detector (TCD), electron capture detector (ECD), or mass spectrometer (MS). Gas chromatography is widely used in fields such as chemistry, biochemistry, environmental science, forensics, and food analysis.

Methyl parathion is an organophosphate insecticide and acaricide. It functions by inhibiting the enzyme cholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine, causing nervous system excitation and ultimately damage or death in insects. However, it can also have toxic effects on mammals, including humans, if ingested, inhaled, or absorbed through the skin. It is classified as a highly hazardous pesticide by the World Health Organization (WHO) and its use is restricted or banned in many countries due to its high toxicity and environmental persistence.

Carboxylic ester hydrolases are a class of enzymes that catalyze the hydrolysis of ester bonds in carboxylic acid esters, producing alcohols and carboxylates. This group includes several subclasses of enzymes such as esterases, lipases, and thioesterases. These enzymes play important roles in various biological processes, including metabolism, detoxification, and signal transduction. They are widely used in industrial applications, such as the production of biodiesel, pharmaceuticals, and food ingredients.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Nitric Oxide Synthase Type III (NOS-III), also known as endothelial Nitric Oxide Synthase (eNOS), is an enzyme responsible for the production of nitric oxide (NO) in the endothelium, the lining of blood vessels. This enzyme catalyzes the conversion of L-arginine to L-citrulline, producing NO as a byproduct. The release of NO from eNOS plays an important role in regulating vascular tone and homeostasis, including the relaxation of smooth muscle cells in the blood vessel walls, inhibition of platelet aggregation, and modulation of immune function. Mutations or dysfunction in NOS-III can contribute to various cardiovascular diseases such as hypertension, atherosclerosis, and erectile dysfunction.

Stereoisomerism is a type of isomerism (structural arrangement of atoms) in which molecules have the same molecular formula and sequence of bonded atoms, but differ in the three-dimensional orientation of their atoms in space. This occurs when the molecule contains asymmetric carbon atoms or other rigid structures that prevent free rotation, leading to distinct spatial arrangements of groups of atoms around a central point. Stereoisomers can have different chemical and physical properties, such as optical activity, boiling points, and reactivities, due to differences in their shape and the way they interact with other molecules.

There are two main types of stereoisomerism: enantiomers (mirror-image isomers) and diastereomers (non-mirror-image isomers). Enantiomers are pairs of stereoisomers that are mirror images of each other, but cannot be superimposed on one another. Diastereomers, on the other hand, are non-mirror-image stereoisomers that have different physical and chemical properties.

Stereoisomerism is an important concept in chemistry and biology, as it can affect the biological activity of molecules, such as drugs and natural products. For example, some enantiomers of a drug may be active, while others are inactive or even toxic. Therefore, understanding stereoisomerism is crucial for designing and synthesizing effective and safe drugs.

Gas Chromatography-Mass Spectrometry (GC-MS) is a powerful analytical technique that combines the separating power of gas chromatography with the identification capabilities of mass spectrometry. This method is used to separate, identify, and quantify different components in complex mixtures.

In GC-MS, the mixture is first vaporized and carried through a long, narrow column by an inert gas (carrier gas). The various components in the mixture interact differently with the stationary phase inside the column, leading to their separation based on their partition coefficients between the mobile and stationary phases. As each component elutes from the column, it is then introduced into the mass spectrometer for analysis.

The mass spectrometer ionizes the sample, breaks it down into smaller fragments, and measures the mass-to-charge ratio of these fragments. This information is used to generate a mass spectrum, which serves as a unique "fingerprint" for each compound. By comparing the generated mass spectra with reference libraries or known standards, analysts can identify and quantify the components present in the original mixture.

GC-MS has wide applications in various fields such as forensics, environmental analysis, drug testing, and research laboratories due to its high sensitivity, specificity, and ability to analyze volatile and semi-volatile compounds.

nitroprusside (ni-troe-rus-ide)

A rapid-acting vasodilator used in the management of severe hypertension, acute heart failure, and to reduce afterload in patients undergoing cardiac surgery. It is a potent arterial and venous dilator that decreases preload and afterload, thereby reducing myocardial oxygen demand. Nitroprusside is metabolized to cyanide, which must be monitored closely during therapy to prevent toxicity.

Pharmacologic class: Peripheral vasodilators

Therapeutic class: Antihypertensives, Vasodilators

Medical Categories: Cardiovascular Drugs, Hypertension Agents

Esterification is a chemical reaction that involves the conversion of an alcohol and a carboxylic acid into an ester, typically through the removal of a molecule of water. This reaction is often catalyzed by an acid or a base, and it is a key process in organic chemistry. Esters are commonly found in nature and are responsible for the fragrances of many fruits and flowers. They are also important in the production of various industrial and consumer products, including plastics, resins, and perfumes.

Fatty acids are carboxylic acids with a long aliphatic chain, which are important components of lipids and are widely distributed in living organisms. They can be classified based on the length of their carbon chain, saturation level (presence or absence of double bonds), and other structural features.

The two main types of fatty acids are:

1. Saturated fatty acids: These have no double bonds in their carbon chain and are typically solid at room temperature. Examples include palmitic acid (C16:0) and stearic acid (C18:0).
2. Unsaturated fatty acids: These contain one or more double bonds in their carbon chain and can be further classified into monounsaturated (one double bond) and polyunsaturated (two or more double bonds) fatty acids. Examples of unsaturated fatty acids include oleic acid (C18:1, monounsaturated), linoleic acid (C18:2, polyunsaturated), and alpha-linolenic acid (C18:3, polyunsaturated).

Fatty acids play crucial roles in various biological processes, such as energy storage, membrane structure, and cell signaling. Some essential fatty acids cannot be synthesized by the human body and must be obtained through dietary sources.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

Methyl methanesulfonate (MMS) is not a medication, but rather a chemical compound with the formula CH3SO3CH3. It's an alkylating agent that is used in laboratory settings for various research purposes, including as a methylating agent in biochemical and genetic studies.

MMS works by transferring its methyl group (CH3) to other molecules, which can result in the modification of DNA and other biological macromolecules. This property makes it useful in laboratory research, but it also means that MMS is highly reactive and toxic. Therefore, it must be handled with care and appropriate safety precautions.

It's important to note that MMS is not used as a therapeutic agent in medicine due to its high toxicity and potential to cause serious harm if mishandled or misused.

Cholesteryl ester transfer proteins (CETP) are a group of plasma proteins that play a role in the transport and metabolism of lipids, particularly cholesteryl esters and triglycerides, between different lipoprotein particles in the bloodstream. These proteins facilitate the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL), while simultaneously promoting the transfer of triglycerides in the opposite direction, from VLDL and LDL to HDL.

The net effect of CETP activity is a decrease in HDL cholesterol levels and an increase in LDL and VLDL cholesterol levels. This shift in lipoprotein composition can contribute to the development of atherosclerosis and cardiovascular disease, as lower HDL cholesterol levels and higher LDL cholesterol levels are associated with increased risk for these conditions.

Inhibition of CETP has been investigated as a potential strategy for increasing HDL cholesterol levels and reducing the risk of cardiovascular disease. However, clinical trials with CETP inhibitors have shown mixed results, and further research is needed to determine their safety and efficacy in preventing cardiovascular events.

Vasodilator agents are pharmacological substances that cause the relaxation or widening of blood vessels by relaxing the smooth muscle in the vessel walls. This results in an increase in the diameter of the blood vessels, which decreases vascular resistance and ultimately reduces blood pressure. Vasodilators can be further classified based on their site of action:

1. Systemic vasodilators: These agents cause a generalized relaxation of the smooth muscle in the walls of both arteries and veins, resulting in a decrease in peripheral vascular resistance and preload (the volume of blood returning to the heart). Examples include nitroglycerin, hydralazine, and calcium channel blockers.
2. Arterial vasodilators: These agents primarily affect the smooth muscle in arterial vessel walls, leading to a reduction in afterload (the pressure against which the heart pumps blood). Examples include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and direct vasodilators like sodium nitroprusside.
3. Venous vasodilators: These agents primarily affect the smooth muscle in venous vessel walls, increasing venous capacitance and reducing preload. Examples include nitroglycerin and other organic nitrates.

Vasodilator agents are used to treat various cardiovascular conditions such as hypertension, heart failure, angina, and pulmonary arterial hypertension. It is essential to monitor their use carefully, as excessive vasodilation can lead to orthostatic hypotension, reflex tachycardia, or fluid retention.

Methylation, in the context of genetics and epigenetics, refers to the addition of a methyl group (CH3) to a molecule, usually to the nitrogenous base of DNA or to the side chain of amino acids in proteins. In DNA methylation, this process typically occurs at the 5-carbon position of cytosine residues that precede guanine residues (CpG sites) and is catalyzed by enzymes called DNA methyltransferases (DNMTs).

DNA methylation plays a crucial role in regulating gene expression, genomic imprinting, X-chromosome inactivation, and suppression of repetitive elements. Hypermethylation or hypomethylation of specific genes can lead to altered gene expression patterns, which have been associated with various human diseases, including cancer.

In summary, methylation is a fundamental epigenetic modification that influences genomic stability, gene regulation, and cellular function by introducing methyl groups to DNA or proteins.

Nitric oxide (NO) donors are pharmacological agents that release nitric oxide in the body when they are metabolized. Nitric oxide is a molecule that plays an important role as a signaling messenger in the cardiovascular, nervous, and immune systems. It helps regulate blood flow, relax smooth muscle, inhibit platelet aggregation, and modulate inflammatory responses.

NO donors can be used medically to treat various conditions, such as hypertension, angina, heart failure, and pulmonary hypertension, by promoting vasodilation and improving blood flow. Some examples of NO donors include nitroglycerin, isosorbide dinitrate, sodium nitroprusside, and molsidomine. These drugs work by releasing nitric oxide slowly over time, which then interacts with the enzyme soluble guanylate cyclase to produce cyclic guanosine monophosphate (cGMP), leading to relaxation of smooth muscle and vasodilation.

It is important to note that NO donors can have side effects, such as headache, dizziness, and hypotension, due to their vasodilatory effects. Therefore, they should be used under the guidance of a healthcare professional.

... ng-nitroarginine methyl ester MeSH D12.125.068.050.587 - nitroarginine MeSH D12.125.068.050.650 - omega-n-methylarginine MeSH ... ng-nitroarginine methyl ester MeSH D12.125.095.104.587 - nitroarginine MeSH D12.125.095.104.650 - omega-n-methylarginine MeSH ... tosylarginine methyl ester MeSH D12.125.068.060 - asparagine MeSH D12.125.068.330 - glutamine MeSH D12.125.068.330.700 - ... tosylarginine methyl ester MeSH D12.125.095.165 - asparagine MeSH D12.125.095.226 - citrulline MeSH D12.125.095.307 - ...
Amino Acids, Diamino - NG-Nitroarginine Methyl Ester PubMed MeSh Term *Overview. Overview. subject area of * Aging compounds ...
NG-Nitroarginine Methyl Ester / pharmacology * Perfusion / methods* * Permeability * Rabbits * Serotonin / pharmacology* * Time ...
NG-Nitroarginine Methyl Ester / pharmacology * Nitric Oxide / antagonists & inhibitors* * Nitric Oxide / physiology ... arginine methyl ester (LNAME, 15-300 nmol/0.2 microl), N (G)-nitro-L: -arginine (LNOARG, 50-300 nmol/0.2 microl), 7- ...
... ng-nitroarginine methyl ester MeSH D12.125.068.050.587 - nitroarginine MeSH D12.125.068.050.650 - omega-n-methylarginine MeSH ... ng-nitroarginine methyl ester MeSH D12.125.095.104.587 - nitroarginine MeSH D12.125.095.104.650 - omega-n-methylarginine MeSH ... tosylarginine methyl ester MeSH D12.125.068.060 - asparagine MeSH D12.125.068.330 - glutamine MeSH D12.125.068.330.700 - ... tosylarginine methyl ester MeSH D12.125.095.165 - asparagine MeSH D12.125.095.226 - citrulline MeSH D12.125.095.307 - ...
Ng-Nitroarginine Methyl Ester. 7. Papers. *. Rosiglitazone. 7. Papers. *. Homocysteine. 6. Papers ...
Ng-Nitroarginine Methyl Ester. 4. Papers. *. Probucol. 4. Papers. *. Rosuvastatin. 4. Papers ...
N(G)-Nitroarginine Methyl Ester N(omega)-Nitro-L-arginine Methyl Ester NG-Nitro-L-Arginine Methyl Ester NG-Nitroarginine Methyl ... use NG-NITROARGININE METHYL ESTER (NM) to search N(G)-NITROARGININE METHYL ESTER 1990-96. History Note. 97; was N(G)- ... NG-Nitroarginine Methyl Ester, D-Orn-Isomer Narrower Concept UI. M0329191. Registry Number. 141968-19-6. Terms. NG- ... NG-Nitroarginine Methyl Ester, L-Orn-Isomer, Monohydrochloride Preferred Term Term UI T359386. Date09/13/1999. LexicalTag NON. ...
NG-Nitroarginine Methyl Ester 22% * Mitochondrial Membrane Potential 20% * Brain Injuries 19% ...
NG-Nitroarginine Methyl Ester. A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce ... WalkerNG-Nitroarginine Methyl EsterMuscle, SkeletalTissue AdhesionsEthylene GlycolNitric Oxide SynthaseAvoidance Learning ... OxideAndrosteroneCorticosteroneCatalaseInsulinSuperoxide DismutaseAspartate AminotransferasesNG-Nitroarginine Methyl Ester ...
NG-Nitroarginine Methyl Ester * NITROPRUSSIDE * Phenylephrine * Random Allocation * Soft Tissue Injuries * Vasoconstrictor ... to cumulative addition of phenylephrine was recorded in the absence and presence of 1 microM NG-nitro-L-arginine methyl ester ( ...
NG-Nitroarginine Methyl Ester 14% * Bromodeoxyuridine 13% * Spectrum Analysis 12% * Messenger RNA 7% ...
NG-Nitroarginine Methyl Ester 27% * Proteins 26% * High-Temperature Requirement A Serine Peptidase 2 22% ...
NG-Nitroarginine Methyl Ester 8% * Nitroprusside 8% * Gene Deletion 8% * Site-Directed Mutagenesis 8% ...
NG-Nitroarginine Methyl Ester 37% 5 Citas (Scopus) * Hypothalamo-hypophyso-gonadal response to clomiphene citrate at median ...
NG-Nitroarginine Methyl Ester 18% * Phenylephrine 17% * Verapamil 17% * Thoracic Aorta 16% ...
NG-Nitroarginine Methyl Ester / pharmacology; Nitric Oxide Synthase / antagonists & inhibitors; Prospective Studies; Swine; ... Effect of N-G-nitro-L-arginine-methyl-ester on cardiopulmonary function and biosynthesis of cyclooxygenase products during ...
NG-Nitroarginine Methyl Ester 45% * Arginine 24% * Prosencephalon 21% * Anesthesia 20% * Cerebellum 18% ...
L-NG-Nitro arginine methyl ester (L-NAME); Low density lipoprotein (LDL); Mammalian target of rapamycin (mTOR); Mas-related G ...
NG-Nitroarginine Methyl Ester Medicine & Life Sciences 27% * Cyclooxygenase 2 Medicine & Life Sciences 19% ...
NG-Nitroarginine Methyl Ester Medicine & Life Sciences 94% * Nitric Oxide Synthase Medicine & Life Sciences 80% ... nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), and an NO precursor, L-arginine. Rats were trained on a ... nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), and an NO precursor, L-arginine. Rats were trained on a ... nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), and an NO precursor, L-arginine. Rats were trained on a ...
... mice chronically treated with the NOS inhibitor l-NG-nitroarginine methyl ester (L-NAME). We confirm that TG2 activity is ... mice chronically treated with the NOS inhibitor l-NG-nitroarginine methyl ester (L-NAME). We confirm that TG2 activity is ... mice chronically treated with the NOS inhibitor l-NG-nitroarginine methyl ester (L-NAME). We confirm that TG2 activity is ... mice chronically treated with the NOS inhibitor l-NG-nitroarginine methyl ester (L-NAME). We confirm that TG2 activity is ...
NG-Nitroarginine Methyl Ester Medicine & Life Sciences 91% * Renin-Angiotensin System Medicine & Life Sciences 83% ... subsequent worsening of hypertension and renal injury induced by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L- ... subsequent worsening of hypertension and renal injury induced by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L- ... subsequent worsening of hypertension and renal injury induced by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L- ...
NG-Nitroarginine Methyl Ester, Neuronal Plasticity, Neurons, Nitric Oxide, Nitric Oxide Synthase Type II, Rats, Signal ...
... water with NG-Nitroarginine Methyl Ester def: "Drinking water with a specified concentration of NG-Nitroarginine Methyl Ester ( ... NG-nitroarginine methyl ester def: "A basic amino acid, commonly known as L-NAME, used as a non-selective inhibitor of nitric ... controlled NG-nitroarginine methyl ester content drinking water def: "A drink made up of water and a specified amount of the ... NG-nitroarginine methyl ester created_by: JSmith creation_date: 2013-03-13T14:48:31Z [Term] id: XCO:0000286 name: retinal S- ...
NG-Nitroarginine Methyl Ester, Neuronal Plasticity, Neurons, Nitric Oxide, Nitric Oxide Synthase Type II, Rats, Signal ...
... then NG-nitroarginine methyl ester (100 umol/l) (for 0.2 hours) then acetylcholine (3.16 umol/l) Spradley FT, et al., Am J ... then NG-nitroarginine methyl ester (100 umol/l) (for 0.2 hours) then acetylcholine (31.6 umol/l) Spradley FT, et al., Am J ... then NG-nitroarginine methyl ester (100 umol/l) then acetylcholine (3.16 umol/l) Spradley FT, et al., Am J Physiol Regul Integr ... then NG-nitroarginine methyl ester (100 umol/l) then acetylcholine (3.16 umol/l) Spradley FT, et al., Am J Physiol Regul Integr ...
NG-Nitroarginine Methyl Ester, Nifedipine, Nitric Oxide Synthase, Nitroarginine, Norepinephrine, Prostaglandin Endoperoxides, ...
  • Smooth muscle contraction in response to cumulative addition of phenylephrine was recorded in the absence and presence of 1 microM NG-nitro-L-arginine methyl ester (L -NAME). (tamu.edu)
  • We investigated the role of nitric oxide (NO) in learning and memory formation in a radial maze test, by using the NO synthase (NOS) inhibitors, N(G)-nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole (7-NI), and an NO precursor, L-arginine. (fujita-hu.ac.jp)
  • The aims of this study were 1) to examine if transient exposure to an angiotensin receptor blocker (ARB) during an early period in hypertension development confers protection against subsequent worsening of hypertension and renal injury induced by the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME), and 2) conversely, to examine the effects of transient exposure to angiotensin II (Ang II) during the same period. (elsevierpure.com)
  • Slices were not treated or were pretreated with 27 microM L-nitroarginine methyl ester (L-NAME), 27 microM 7-nitroindozole (7-NI), or 27 microM L-nitroarginine. (asahq.org)
  • El propósito del presente estudio fue investigar a través de análisis bioquímicos, los efectos de la exposición a formaldehído, que podría causar estrés oxidativo, en el corazón y la aorta. (bvsalud.org)
  • We then demonstrate that endothelium-derived bioactive NO primarily mediates its effects through TG2, using TG2 -/- mice chronically treated with the NOS inhibitor l-N G -nitroarginine methyl ester (L-NAME). (johnshopkins.edu)
  • LV superoxide (O(2)(·-)) production was increased in nNOS(-/-) mice and reduced by L-N(ω)-nitroarginine methyl ester (L-NAME), indicating uncoupling of eNOS activity. (ox.ac.uk)