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.
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.
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)
A 30-kDa COMPLEMENT C1Q-related protein, the most abundant gene product secreted by FAT CELLS of the white ADIPOSE TISSUE. Adiponectin modulates several physiological processes, such as metabolism of GLUCOSE and FATTY ACIDS, and immune responses. Decreased plasma adiponectin levels are associated with INSULIN RESISTANCE; TYPE 2 DIABETES MELLITUS; OBESITY; and ATHEROSCLEROSIS.
Cell surface receptors for ADIPONECTIN, an antidiabetic hormone secreted by ADIPOCYTES. Adiponectin receptors are membrane proteins with multiple cytoplasmic and extracellular regions. They are about 43 kDa and encoded by at least two genes with different affinities for globular and full-length adiponectin.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
The figwort plant family of the order Lamiales. The family is characterized by bisexual flowers with tubular corollas (fused petals) that are bilaterally symmetrical (two-lips) and have four stamens in most, two of which are usually shorter.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
Rod-shaped storage granules for VON WILLEBRAND FACTOR specific to endothelial cells.
Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the CELL MEMBRANE.
ATPases that are members of the AAA protein superfamily (ATPase family Associated with various cellular Activities). The NSFs functions, acting in conjunction with SOLUBLE NSF ATTACHMENT PROTEINS (i.e. SNAPs, which have no relation to SNAP 25), are to dissociate SNARE complexes.
A superfamily of small proteins which are involved in the MEMBRANE FUSION events, intracellular protein trafficking and secretory processes. They share a homologous SNARE motif. The SNARE proteins are divided into subfamilies: QA-SNARES; QB-SNARES; QC-SNARES; and R-SNARES. The formation of a SNARE complex (composed of one each of the four different types SNARE domains (Qa, Qb, Qc, and R)) mediates MEMBRANE FUSION. Following membrane fusion SNARE complexes are dissociated by the NSFs (N-ETHYLMALEIMIDE-SENSITIVE FACTORS), in conjunction with SOLUBLE NSF ATTACHMENT PROTEIN, i.e., SNAPs (no relation to SNAP 25.)
SNARE binding proteins that facilitate the ATP hydrolysis-driven dissociation of the SNARE complex. They are required for the binding of N-ETHYLMALEIMIDE-SENSITIVE PROTEIN (NSF) to the SNARE complex which also stimulates the ATPASE activity of NSF. They are unrelated structurally to SNAP-25 PROTEIN.
A broad category of proteins involved in the formation, transport and dissolution of TRANSPORT VESICLES. They play a role in the intracellular transport of molecules contained within membrane vesicles. Vesicular transport proteins are distinguished from MEMBRANE TRANSPORT PROTEINS, which move molecules across membranes, by the mode in which the molecules are transported.
A plant species of the family CUCURBITACEAE. It is a source of ribosome-inactivating proteins and triterpene glycosides.
A publication issued at stated, more or less regular, intervals.
Print and non-print materials collected, processed, and stored by libraries. They comprise books, periodicals, pamphlets, reports, microforms, maps, manuscripts, motion pictures, and all other forms of audiovisual records. (Harrod, The Librarians' Glossary, 4th ed, p497)
Individual's rights to obtain and use information collected or generated by others.
A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.
A plant genus of the family CUCURBITACEAE. It is a source of momordin.
The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)
The restoration to life or consciousness of one apparently dead. (Dorland, 27th ed)
Diversion of the flow of blood from the pulmonary veins directly to the aorta, avoiding the left atrium and the left ventricle (Dorland, 27th ed). This is a temporary procedure usually performed to assist other surgical procedures.
The artificial substitution of heart and lung action as indicated for HEART ARREST resulting from electric shock, DROWNING, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation (RESPIRATION, ARTIFICIAL) and closed-chest CARDIAC MASSAGE.
Specialized hospital facilities which provide diagnostic and therapeutic services for trauma patients.
Volume of circulating BLOOD. It is the sum of the PLASMA VOLUME and ERYTHROCYTE VOLUME.
Therapy whose basic objective is to restore the volume and composition of the body fluids to normal with respect to WATER-ELECTROLYTE BALANCE. Fluids may be administered intravenously, orally, by intermittent gavage, or by HYPODERMOCLYSIS.

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)

Isolated perfused mesenteric arteries of portal vein ligated and sham-operated rats were contracted by methoxamine (3 nmol-3 mumol) and then treated with nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (100 microM), terlipressin or the selective V2 receptor agonist desmopressin (each 0.5 uM). Terlipressin alone reduced and in combination with NG-nitro-L-arginine methyl ester abolished the difference in reactivity to methoxamine between the portal vein ligated and sham-operated groups ...
A role for the NO-cGMP pathway in mediating chemosensory activation of feeding is suggested by intense NADPH diaphorase staining observed in nerve fibers that project from sensory cells in the lips to the CNS and by the presence in the CNS of a NO-activated guanylyl cyclase. In preparations reduced to isolated lips and CNS, intracellular recordings were made from motoneurons driven by the interneurons of the central pattern generator (CPG) for feeding. Fictive feeding in such preparations can be recorded from these motoneurons following the application of sucrose to the lips. Sucrose activation of fictive feeding is inhibited by the NO scavenger hemoglobin, the NO synthase inhibitor N omega-Nitro-L-Arginine Methyl Ester (L-NAME) and by methylene blue, an inhibitor of guanylyl cyclase. Fictive feeding in isolated lip-CNS preparations can be activated without sucrose by superfusion of NO donor molecules such as SNAP and hydroxylamine and by the nonhydrolyzable analog of cGMP, 8-bromo-cGMP. The ...
Alfa Aesar™ D-Methionine methyl ester hydrochloride, 98% 100g Alfa Aesar™ D-Methionine methyl ester hydrochloride, 98% Amino Acids
In the present study, chronic administration of bosentan, an antagonist of both ETA and ETB receptors, had no significant effect on the systolic BP level reached after 6 weeks of L-NAME treatment, confirming the observation that acute (60 minutes) administration of the selective ETA receptor antagonist BQ-123 could not lower BP in rats treated for 3 weeks with an l-arginine analogue.21 However, the delay in the BP elevation occurring when bosentan was added to L-NAME would suggest that ET is involved in the early hypertensive response to the l-arginine analogue. This observation is in line with studies showing a blunted hypertensive effect of acute L-NAME administrations by ET receptor antagonists12 13 14 and provides experimental evidence to explain the discrepancy in the efficacy of ET receptor antagonists in acute and chronic L-NAME-induced hypertension.. Chronic administration of L-NAME leads to eutrophic remodeling of the basilar artery, as we previously reported.15 The structural ...
We manufacture L-Phenylalanine methyl ester hydrochloride CAS:7524-50-7 from China India,methyl (2S)-2-amino-3-phenylpropanoate,hydrochloride factory and L-Phenylalanine, methyl ester, hydrochloride (1:1) producer,L-Phenylalanine methyl ester hydrochloride manufacturer and supplier
The report generally describes d-leucine methyl ester hydrochloride, examines its uses, production methods, patents. D-Leucine methyl ester hydrochloride
The purpose of this study was to examine the effects of nitric oxide on systemic hemodynamics and oxygen metabolism following acute hepatic inflow occlusion. Fourteen mongrel pigs received solvent (control group, n = 4), the nitric synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME group, n = 5), or the substrate for nitric oxide synthesis L-arginine (L-arginine group, n = 5) 30 min before hepatic inflow occlusion. Following 30 min of hepatic ischemia, all livers were reperfused. While all pigs in the control group and L-arginine group survived more than 7 days after reperfusion, two of five pigs in the L-NAME group died during hepatic ischemia period. However, venous oxygen saturation was significantly lower during and after ischemic period, oxygen extraction ratio was significantly higher during hepatic ischemic period in L-NAME group, and systemic vascular resistance was also significantly higher 5 and 15 min after hepatic inflow occlusion. Furthermore, lactate/pyruvate ratio was ...
Advances in Pharmacological and Pharmaceutical Sciences is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies in all areas of experimental and clinical pharmacology, pharmaceutics, medicinal chemistry and drug delivery.
Examination of the protective effect of L-NAME(N-Nitro L-Arginine Methyl Ester) and vitamin E (α-tocopherol) against oxidative stress caused by exposure of cigarette smoke to lungs in male rats ...
Capot Chemical CAS# 13515-97-4, DL-Alanine methyl ester hydrochloride. 13515-97-4 MSDS,ROS,13515-97-4 MOA,COA,SPECS,pecifications,1H-NMR,GHS,CAT #10905;Methyl DL-2-aminopropanoate hydrochloride
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TY - JOUR. T1 - Vaccination against the angiotensin type 1 receptor for the prevention of L-NAME-induced nephropathy. AU - Azegami, Tatsuhiko. AU - Sasamura, Hiroyuki. AU - Hayashi, Kaori. AU - Itoh, Hiroshi. PY - 2012/5. Y1 - 2012/5. N2 - Previous studies have shown that renin-angiotensin (Ang) system vaccines may be effective for the treatment of hypertension, but their efficacy for the prevention of renal disease is unclear. The aim of this study was to compare the effects of an Ang II type 1 (AT1) receptor vaccine with an Ang II receptor blocker (ARB) and a vasodilator on blood pressure (BP) and renal injury in the L-NAME nephropathy model. Male spontaneously hypertensive rats (SHRs) were divided into six groups and treated transiently with three injections of vehicle or AT1 receptor vaccine (0.1 mg) at age 4, 6 and 8 weeks, or continuously with candesartan cilexetil (0.1 mg kg -1 per day) or hydralazine hydrochloride (5 mg kg -1 per day), then administered NG-nitro-L-arginine methyl ester ...
Product Number , 58089751. CAS Number , 5874-57-7. EC , Molecular Formula , -. Molecular Weight , 155.58. Storage Temp , Harmonized Tariff code , Signal Word , ...
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m-Propoxycarbanilic acid 2-(dimethylamino)ethyl ester hydrochloride | C14H23ClN2O3 | CID 50044 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
o-Mercaptobenzoic acid 3-(2-methylpiperidino)propyl ester hydrochloride | C16H24ClNO2S | CID 48992 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
The intracellular signaling of human urotensin II (hU-II) and its interaction with other vasoconstrictors such as ANG II are poorly understood. In endothelium-denuded rat aorta, coadministration of hU-II (1 nM) and ANG II (2 nM) exerted a significant contractile effect that was associated with increased protein kinase C (PKC) activity and phosphorylation of PKC-α/βII and myosin light chain, whereas either hU-II or ANG II administered alone at these concentrations had no statistically significant effect. This synergistic effect was abrogated by the PKC inhibitor chelerythrine (10 and 30 μM), the selective PKC-α/βII inhibitor Gö-6976 (0.1 and 1 μM), the hU-II receptor ligand urantide (30 nM and 1 μM), or the ANG II antagonist losartan (1 μM). Moreover, in endothelium-intact rat aorta, the synergistic effect of hU-II and ANG II was not exerted any longer, and this synergistic effect was unmasked by pretreatment of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester. hU-II ...
Effects of Nerve Growth Factor and Nitric Oxide Synthase Inhibitors on Amyloid Precursor Protein mRNA Levels and Protein Stability
TY - JOUR. T1 - Linalool elicits vasorelaxation of mouse aortae through activation of guanylyl cyclase and K+ channels. AU - Kang, Purum. AU - Seol, Geun Hee. N1 - Publisher Copyright: © 2015 Royal Pharmaceutical Society.. PY - 2015/5/1. Y1 - 2015/5/1. N2 - Objectives The aim of this study was to investigate the cardiovascular relaxing properties of monoterpene alcohol (-)-linalool (LIN), a principal component of several aromatic plants. Methods We assessed the effects of LIN on vascular contractility in mouse aortae and evaluated its underlying mechanisms of action. Key findings We found that LIN dose-dependently relaxed the vascular tonus of mouse thoracic aortae induced by prostaglandin F2 alpha (PGF2α, 3 μm). This effect, however, was reduced by pretreatment with the nitric oxide synthase inhibitor L-NAME (30 μm). Treatment with the inhibitor of soluble guanylyl cyclase ODQ (2 μm) or the K+ channel blocker TEA (10 mM) partially blocked LIN-induced vasorelaxation. Moreover, addition of ...
Of all cancer types, prostate cancer is the second most common one with an age-standardized incidence rate of 29.3 per 100,000 men worldwide. Nitric oxide (NO) is both a radical and versatile messenger molecule involved in many physiological activities. NO was documented to be highly secreted and utilized by cancer cells. N omega-nitro-l-arginine methyl ester (L-NAME) is utilized for inhibiting NO synthase. Its worst long-term side effect is reported to be hypertension, hence less cytotoxic than chemotherapeutic agents. Herein, we carried out a cytotoxicity study on how different doses of L-NAME affect DU145 human prostate cancer cells. First, toxic doses of L-NAME were determined. Then, while antioxidant capacity was determined by glutathione and total antioxidant status, oxidative stress was evaluated by quantifying malondialdehyde, NO, and total oxidant status levels. Inflammatory effects of L-NAME were investigated by measuring tumor necrosis factor-alpha and interleukin-6 (IL-6) levels. ...
This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS
MACIEL, IZAQUE DE SOUSA... Nitric Oxide Synthase inhibition counteracts the stress-induced DNA methyltransferase 3b expression in the hippocampus of rats. European Journal of Neuroscience n. p. DEC 2020. Journal article.
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Previous studies identified a region on chromosome 1 associated with NG-nitro-L-arginine methyl ester (L-NAME) hypertension-induced renal disease in fawn-hooded hypertensive (FHH) rats. This region contains a mutant γ-adducin (Add3) gene that impairs renal blood flow (RBF) autoregulation, but its contribution to renal injury is unknown. The present study evaluated the hypothesis that knockout (KO) of Add3 impairs the renal vasoconstrictor response to the blockade of nitric oxide synthase and enhances hypertension-induced renal injury after chronic administration of L-NAME plus a high-salt diet. The acute hemodynamic effect of L-NAME and its chronic effects on hypertension and renal injury were compared in FHH 1Brown Norway (FHH 1BN) congenic rats (WT) expressing wild-type Add3 gene versus FHH 1BN Add3 KO rats. RBF was well autoregulated in WT rats but impaired in Add3 KO rats. Acute administration of L-NAME (10 mg/kg) raised mean arterial pressure (MAP) similarly in both strains, but RBF and ...
ABSTRACT Objective: To evaluate the role of nitric oxide (NO) in pioglitazone (PIO) mediated anti-inflammatory activity in ulcerative colitis. Material and methods: Ulcerative colitis was induced in rats by intracolonical administration of 2, 4, 6-tri-nitrobenzene sulphonic acid (50mg/rat) after 10 days of initiation of treatment except in vehicle control group. Animals were randomly divided into five groups with six animals each. The groups received vehicle, TNBS, PIO, PIO+L-NAME (N-nitro-L-arginine methyl ester), L-NAME for 18 days respectively. PIO (25 mg/kg/day p.o) treatment for 18 days reduced mucosal damage induced by TNBS which was reflected by improvement in body weight, morphological grades of colon, reduced myeloperoxidase activity and histopathological studies. Administration of L-NAME (40 mg/kg/day, p.o) for 18 days in PIO+TNBS treated animals showed exaggerated mucosal damage as compared to PIO+TNBS treated animals. Results: Findings indicate that L-NAME altered the protective ...
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The present results showed that i.p. administration of IL-1β in freely moving rats induced a biphasic increase in mean arterial blood pressure, and that a rise in the plasma concentration of NOx occurred during the second phase of the pressor response (at 3 h after the injection of IL-1β). Furthermore, systemic pretreatment with DEX enhanced the second phase of the pressor response, thus confirming our previous finding (Watanabe et al., 1996), and inhibited the evoked increase in the plasma level of NOx. These results suggest that NO is involved as a vasodilator in the regulation of the late phase of the pressor response, and that the enhancement by DEX of the IL-1-induced rise in blood pressure was, at least in part, due to its inhibition of NO release. This idea is further supported by the finding that one of the most frequently used nonselective NOS inhibitors,l-NAME, both enhanced the IL-1β-induced pressor response and attenuated the NOx response seen in this study. This result indicates ...
ROSSI, Marcos Antonio. Chronic inhibition of no synthesis per se promotes structural animal remodeling of the rat aorta. Anais.. Washington: [s.n.], 2001 ...
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Applications of Algebra in Dance Composition. This workshop will explore how dance composition can get analytical, precise, and even mathematical- but by no means boring! Regular polyhedra are often used in dance as a means of orienting yourself in space, and in this workshop we will see how algebraic concepts on the vertices of these figures can be related to choreographic devices in dance composition. We will also uncover a way of crafting variations on your own phrase of choreographic work with math!. Bridges Movie Festival. A selection of videos conveying mathematical ideas and ways of thinking. If you like Vi Harts math videos, youll enjoy this collection by a variety of video artists.. Divergence of Sinusoidal Vector Fields: Sources of Flow as Sources of Symmetry. Using the divergence of a vector field we create black and white symmetric patterns resembling patterns commonly found on textiles and baskets. We focus on sinusoidal vector fields of the form because of the interesting ...
... ng-nitroarginine methyl ester MeSH D12. - nitroarginine MeSH D12. - omega-n-methylarginine MeSH ... ng-nitroarginine methyl ester MeSH D12. - nitroarginine MeSH D12. - 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 - ...
Further, the nitric oxide inhibitor (NO), L-Nomega - nitro-Arginine Methyl Ester (L-NAME) 10 mg/kg totally inhibited the rise ... The pressor dose response characteristic of CCD-X on PMV was similar to that of endothelin-1 with EC50 close to 100 ng. It was ...
Nitroarginine methyl ester (NAME). *NCX-456. *NXN-462. *ONO-1714. *VAS-2381 ... Nitroglycerin (NG), also known as nitroglycerine, trinitroglycerin (TNG), nitro, glyceryl trinitrate (GTN), or 1,2,3- ... The nitro group is thus added as an ester C−O−NO2 and water is produced. This is different from an electrophilic aromatic ... Infrequent exposure to high doses of nitroglycerin can cause severe headaches known as "NG head" or "bang head". These ...
N omega-Nitro-L-arginine Methyl Ester; NG-Nitro-L-Arginine Methyl Ester. On-line free medical diagnosis assistant. Ranked list ... NG-Nitroarginine Methyl Ester (L-NAME; N omega-Nitro-L-arginine Methyl Ester; NG-Nitro-L-Arginine Methyl Ester). A non- ...
NG-Nitroarginine Methyl Ester Grant support * DK-53388/DK/NIDDK NIH HHS/United States ... but not the eNOS inhibitor l-nitroarginine methyl ester (l-NAME). Finally, gAd ameliorated the suppression of eNOS activity by ...
NG-Nitroarginine Methyl Ester Grant support * R37 HL41002/HL/NHLBI NIH HHS/United States ...
5.87 ng/g wet weight (P , 0.01) ([Figure 3]).. Figure 2 Effect of l-NG-nitroarginine methyl ester. (l-NAME) and ginkgo biloba ... Effect of treatment with ginkgo biloba extract 761 on the mean blood pressure in l-N G-nitroarginine methyl ester-treated rats ... Effect of l-N G-nitroarginine methyl ester on the mean blood pressure of rats. Before treatment, the systolic BP was 123.30 ± ... Figure 3 Effect of l-NG-nitroarginine methyl ester. (l-NAME) and ginkgo biloba extract 761 (EGb761) on the level of renal tumor ...
The effect of the NOS inhibitor, L-NG-Nitroarginine methyl ester (L-NAME) (100 μM) (Sigma Chemicals, St. Louis, MO, USA), ... inhibition with L-NG-Nitroarginine methyl ester (L-NAME) (100 M). We also evaluated the effect of HO inhibition on ... of nitric oxide synthase inhibition with L-NG-Nitroarginine methyl ester (L-NAME) (100 μM), and of both, on skin blood flow ... and nitric oxide synthase inhibition with L-NG-Nitroarginine methyl ester (L-NAME) (100 μM) on the vasoconstricting effect of ...
L-NG-nitroarginine methyl ester. LXR:. Liver X receptors. MCP-1:. Monocyte chemoattractant protein-1. ... S.-J. Wu and L.-T. Ng, "Antioxidant and free radical scavenging activities of wild bitter melon (Momordica charantia Linn. var ...
l-NG-nitroarginine methyl ester. LP. Lipid peroxidation. MDA. Malondialdehyde. NADPH. Nicotinamide adenine dinucleotide ... nitroarginine binding. J Neurotrauma 16:865-877PubMedCrossRefGoogle Scholar ...
L-NG-Nitroarginine methyl ester. NEM. N-ethylmaleimide. PDB. Protein Database. PRIDE. proteomics identifications database. Prx ... Cells were treated with 1 mm l-NG-Nitroarginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) (90 min), 200 μm Cys ( ...
2149-70-4/Nitroarginine; 362-74-3/Bucladesine; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-45-6/Histamine; 58-15-1/Aminopyrine ... NG-Nitroarginine Methyl Ester / pharmacology. Nitric Oxide / biosynthesis, physiology*. Nitric Oxide Donors / pharmacology. ... Pre-treatment with either of the NOS inhibitors NG-nitro-L-arginine methyl ester (L-NAME) or NG-nitro-L-arginine (L-NNA) ... or equivalent amounts of its biologically inactive enantiomer NG-nitro-D-arginine methyl ester (D-NAME); the NOS inhibitor NG- ...
NG-Nitroarginine methyl ester View Synonyms. View Structure. Description:. A non-selective inhibitor of nitric oxide synthase. ...
NG-Nitroarginine Methyl Ester. Nitric Oxide / physiology*. Rats. Rats, Inbred Strains. Reference Values. Renal Circulation / ... 10102-43-9/Nitric Oxide; 17035-90-4/omega-N-Methylarginine; 50903-99-6/NG-Nitroarginine Methyl Ester; 74-79-3/Arginine ... or N-nitro-L-arginine methylester (NAME; 10 mg/kg body wt) led to a large, sustained rise in blood pressure, a large rise in ...
NG-nitroarginine methyl ester; M1, primary motor cortex; M2, secondary motor cortex; NG, nodose ganglion; NT, not tested; NTS, ... L-Arginine hydrochloride (Arg), L-NG-nitroarginine methyl ester (L-NAME), L-phenylalanine (Phe), and CCK were purchased from ... NG) neurons, where the soma of the vagus nerve is distributed, contain two types of D-glucose-responsive NG neurons. A large ...
NG-Nitroarginine Methyl Ester (pharmacology) *Nitric Oxide (physiology) *Potassium Channels (drug effects) ...
NG-Nitroarginine Methyl Ester (L-NAME) 8. 2- phenyl- 4,4,5,5- tetramethylimidazoline- 1- oxyl- 3- oxide ...
NG-Nitroarginine methyl ester ( l -NAME) (10 µM; eNOS inhibitor), MK-2206 (100 nM; protein kinase B (Akt) inhibitor) sodium ...
The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg iv) attenuated (P , 0.05) antral relaxations and, ... NG-Nitroarginine Methyl Ester. Search for additional papers on this topic. Explore Further: Topics Discussed in This Paper. ...
Journal Article] Tadalafil Improves L-NG-Nitroarginine Methyl Ester-Induced Preeclampsia With Fetal Growth Restriction-Like ...
A nonspecific inhibitor of nitric oxide synthase (NOS), L-NG-Nitroarginine methyl ester (L-NAME; 10 mg/kg IV), was applied ...
Neuroprotective Role of L-NG-Nitroarginine Methyl Ester (L-NAME) against Chronic Hypobaric Hypoxia with Crowding Stress (CHC) ...
NG-Nitroarginine Methyl Ester 17 Citations (Scopus) Oral sapropterin augments reflex vasoconstriction in aged human skin ...
NG-Nitroarginine Methyl Ester Cardiopulmonary Resuscitation Heart Arrest Vasodilator Agents Resuscitation Nitric Oxide ...
L-NG-Nitroarginine Methyl Ester (L-NAME), dimethyl sulfoxide (DMSO), 2′,7′-dichloro-dihydrofluorescein diacetate (H2DCF-DA), 12 ... 2-Cyanoethyl)-6,7,12,13-tetrahydro-13-methyl-5-oxo-5H-indolo(2,3-a)pyrrolo(3,4-c)-carbazole (Gö6976), (+)-5-methyl-10,11- ...
... or L-NG-nitroarginine methyl ester (L-NAME), both used at 1 mM. Ctrl and L-Arg, n = 26; DiMeArg and L-NAME, n = 16; DiMeArg + L ... A and B) Human naive CD4+ T cells were activated in L-Arg medium or Ctrl medium in the presence of 10 ng/mL IL-12. IFN-γ was ...
... ng-nitroarginine methyl ester MeSH D12. - nitroarginine MeSH D12. - omega-n-methylarginine MeSH ... ng-nitroarginine methyl ester MeSH D12. - nitroarginine MeSH D12. - 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 - ...
Vasorelaxant effects of brazilin on endothelium-intact thoracic aorta rings pre-contracted with NE (1 μmol/L) or KCl (60 mmol/L ... NG-Nitroarginine Methyl Ester/pharmacology. *Nitric Oxide Synthase/antagonists & inhibitors. *Phosphorylation/drug effects ... Mentions: Brazilin inhibited the NE (1 μmol/L)-induced sustained contraction in the rat aortic rings in a dose-dependent manner ... Mentions: Brazilin inhibited the NE (1 μmol/L)-induced sustained contraction in the rat aortic rings in a dose-dependent manner ...
The non-isoform specific NOS-inhibitor L-NG-Nitroarginine methyl ester (L-NAME) decreased and an NO-donor compound increased ...
... nitro-L-arginine methyl ester, i.e. L-NAME) were challenged with stable gastric pentadecapeptide BPC 157, which inhibits both ... NG-Nitroarginine Methyl Ester - metabolism, Peptide Fragments - metabolism, Proteins - metabolism. Full Text Order reprints ... The effect of N(G)-nitro-L-arginine methyl ester and L-arginine.. Alenka Boban-Blagaic, Vladimir Blagaic, Zeljko Romic, Nikola ... nitro-L-arginine methyl ester, i.e. L-NAME) were challenged with stable gastric pentadecapeptide BPC 157, which inhibits both ...
NG-Nitroarginine Methyl Ester/pharmacology, Nerve Tissue Proteins/antagonists & inhibitors, Nitric Oxide/*physiology, Nitric ...
Pretreatment of TG mice with the NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 20 mg/kg) abolished the ...
  • Pre-treatment with either of the NOS inhibitors NG-nitro-L-arginine methyl ester (L-NAME) or NG-nitro-L-arginine (L-NNA) enhanced the secretory response. (biomedsearch.com)
  • The effect of N(G)-nitro-L-arginine methyl ester and L-arginine. (medscimonit.com)
  • BACKGROUND: Alcohol disturbances, NO stimulation (by the NO-precursor L-arginine), and/or NO-synthesis blockade (by N(G)-nitro-L-arginine methyl ester, i.e. (medscimonit.com)
  • Further, the nitric oxide inhibitor (NO), L-Nomega - nitro-Arginine Methyl Ester (L-NAME) 10 mg/kg totally inhibited the rise in medullary blood flow due to CCD-X. In vitro studies in isolated perfused kidneys (IPK) and in pressurised microvessels (PMV) confirmed the in vivo effect to cause vasoconstriction, which was inhibited by endothelin A and B antagonists. (wikipedia.org)
  • To compare the nitric oxide synthase (NOS) inhibitors NG-methyl-L-arginine (L-NMA) and aminoguanidine (AG) as prophylactic and therapeutic agents in rat adjuvant induced arthritis (AIA). (elsevier.com)
  • The abilities of L-NMA, AG and another NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), to inhibit NO production by chondrocytes and synoviocytes were also compared. (elsevier.com)
  • We examined the effects of BQ-610, a specific ETA-receptor antagonist, after NO inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) in the anesthetized rat. (qub.ac.uk)
  • The measurements were repeated in the presence of N ω -nitro-L-arginine methyl ester (L-NAME) and indomethacin as nitric oxide synthase (NOS) and cyclooxygenase inhibitors. (elsevier.com)
  • Background: We previously reported that N ω -nitro-L-arginine methyl ester (L-NAME) enhances airway responsiveness to inhaled serotonin in cats treated with atropine and propranolol. (elsevier.com)
  • An inhibitor of endothelium-derived relaxing factor (EDRF) synthase, N ω -nitro-L-arginine methyl ester (L-NAME) (0.65 mM). enhanced the veratridine-induced contraction in rings with an intact endothelium, which suggests that EDRF was being released during the veratridine-induced contraction. (elsevier.com)
  • 3) L-nitro-arginine-methyl esther (L-NAME, 0.5 mg/kg/bw i.v. (elsevier.com)
  • Photorelaxation was not reduced by the nitric oxide synthetase inhibitors, ND-monomethyl-L-arginine (L-NMMA) and N(ω)-nitro-L-arginine methyl ester (L-NAME). (elsevier.com)
  • The levels of N(G)-nitro-L-arginine methylester (L- NAME)-sensitive cyclic GMP (cGMP) in aortas isolated from ZD or ZG were significantly lower than those obtained from control animals. (elsevier.com)
  • The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. (elsevier.com)
  • The CMMCs and smooth muscle spontaneous contractions were significantly decreased by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), an ANO1 channel blocker, and NG-Nitro-L-arginine methyl ester hydrochloride (L-NAME), an inhibitor of nitric oxide synthase activity, in DSS-colitis mice compared with that of control mice. (bvsalud.org)
  • 3) N-nitro-L-arginine methyl ester (L-NAME) 5 mg/kg iv 20 min prior to IL-1β 100 ng icv, followed by L-arginine 150 mg/kg iv (for reversal of L-NAME). (elsevier.com)
  • The NO synthase inhibitor N G -nitro-l-arginine methyl ester (L-NAME) at a per se noneffective dose of 0.3 mg/kg potentiated the inhibitory effects of low doses of LiCl (0.01 and 0.05 mg/kg) on both phases of morphine effect. (elsevier.com)
  • In this study, BF was measured using radiolabeled microspheres during treadmill exercise (10% grade, 20 m/min) before and after NO synthase (NOS) inhibition with N(G)-nitro-L-arginine methyl ester (30 mg/kg ia). (elsevier.com)
  • Since, reactive oxygen species (ROS) and nitric oxide (NO) seem to be responsible for this toxicity , the antioxidant, N-acetyl-L-cysteine (L-NAC), and NO synthetase inhibitor, N-nitro- L-arginine methyl ester ( L-NAME ) were predicted to have protective effects against carboplatin ototoxicity . (bvsalud.org)
  • L-NG-nitro arginine methyl ester (L-NAME) (300 μg/i.c.v./toto) did not induce significant EEG or behavioral changes whereas when injected 15 min before i.c.v. morphine or Deltorphin II (100 μg/icv/toto) dose dependently prevented the EEG ictal episodes, the spiking activity and the synchronized EEG pattern induced by morphine or Deltorphin II. (alliedacademies.org)
  • In fact, the nitric oxide synthase inhibitor L-NG-nitro arginine methyl ester reduces in parallel both NO and prostaglandin generation: this effect is reversed by L-arginine, the precursor for the NO synthesis, but not by D-arginine [ 19 ]. (alliedacademies.org)
  • The effect of L-arginine on NO production was blocked by L-lysine, a basic amino acid that shares the same system y(+) transporter with L-arginine, and by the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). (nih.gov)
  • Endothelial removal, pre-contraction with KCl (40 mM), pre-treatment with tetraethylammonium or with Nω-Nitro-L-arginine methyl ester inhibited the vasodilator response to isoproterenol only in aortic rings from older rats. (elsevierpure.com)
  • We also investigated the effects of a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on the behavioural changes induced by repeated PCP treatment in mice. (fujita-hu.ac.jp)
  • However, N(G)-nitro-D-arginine methyl ester (D-NAME, 50 mg kg -1 day -1 , i.p.), a less active enantiomer of L-NAME, had no effect, suggesting a stereospecific mechanism. (fujita-hu.ac.jp)
  • Signals were significantly reduced by the addition of hemoglobin and by N-nitro-L-arginine methyl ester. (mblwhoilibrary.org)
  • Hypertension was induced in these rats by administering l-N G -nitroarginine methyl ester (l-NAME) (10 mg/kg/day, intraperitoneal) for 12 weeks. (eg.net)
  • Methods: 39 anesthetized female Sprague-Dawley rats were exposed to CN intoxication (5.4 mg/kg intra-arterially) with or without previous nitric oxide synthase (NOS) inhibition by L-NG-nitroarginine methyl ester (L-NAME) injection (40 mg/kg intraperitoneally). (uhms.org)
  • Moreover, both sodium nitroprusside and glyceryl trinitrate en-hance the production of prostaglandins, suggesting that NO stim-ulates prostaglandin biosynthesis through a direct interaction with cyclooxygenase enzymes [ 19 ]. (alliedacademies.org)
  • OxLDL-induced BAEC proliferation and superoxide release were inhibited by the NAD(P)H oxidase inhibitor diphenyleneiodonium (DPI), but not the eNOS inhibitor l-nitroarginine methyl ester (l-NAME). (nih.gov)
  • The effect of the NOS inhibitor, L-NG-Nitroarginine methyl ester (L-NAME) (100 μ M) (Sigma Chemicals, St. Louis, MO, USA), similarly applied by iontophoresis, was then evaluated on another finger. (hindawi.com)
  • Pretreatment of TG mice with the NO synthase inhibitor L-NG-nitroarginine methyl ester (L-NAME, 20 mg/kg) abolished the increase in MRC states 2 and 3 compared to WT. (ahajournals.org)
  • The cellular NO produced by doxycycline treatment also effectively down-regulated CYP2B6 protein, which was blocked by the co-treatment with the NOS2 competitive inhibitor L-NG-nitroarginine methyl ester (L-NAME). (ovid.com)
  • We investigated the efficacy and mechanisms of tadalafil, a selective phosphodiesterase 5 inhibitor, in treating preeclampsia (PE) with fetal growth restriction (FGR) using L-NG-nitroarginine methyl ester (L-NAME)-induced PE with FGR in pregnant mice as our experimental model. (stiffyoverthecountererectionpills.com)
  • Increase in DMSO-induced relaxation in the presence of the endothelium was attenuated by preincubation in L-N-G-nitroarginine methyl ester (L-NAME, 100 mu mol/l) and by the removal of the endothelium. (researchmap.jp)
  • abstract = "Caffeic acid phenethyl ester (CAPE) exerts pharmacological actions (e.g. anti-inflammatory, chemopreventive) which are relevant for potential clinical application in the digestive tract. (elsevier.com)
  • Exercise was associated with lower plasma leptin (192.23 ± 7.22 vs. 169.65 ± 4.6 ng/L) and blood glucose (19.61 ± 0.76 vs. 14.58 ± 0.88 mmol/L) levels. (biomedcentral.com)