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1.
During dormancy of terrestrial snails, the whole neuromodulation of the nervous system is deeply modified. In this work we studied the adaptation of a previously described, putatively nitric oxide (NO) forming enteral network to the long-term resting periods of the snail Helix lucorum. The standard NADPH diaphorase (NADPHd) technique, which is an accepted method for histochemical NO synthase (NOS) detection, labeled the same enteric neurons of the midintestine in active or hibernated snails. Quantification of the NO-derived nitrite by the Griess reaction established that the nitrite formation is confined to the NADPHd-reactive network containing the midintestinal segment. In active snails, the nitrite formation could be enhanced by the NOS substrate l-arginine (10 M–1 mM), but decreased by the known NOS inhibitors 1 mM N-nitro-l-arginine (NOARG) and 10 mM aminoguanidine (AG). Application of 1 mM l-arginine and 1 mM NOARG decreased the amplitude of the midintestinal muscle contractile activity, but did not affect the rectal motility. In dormancy, the nitrite formation was reduced in the NADPHd-reactive midintestinal network. Application of l-arginine could not provoke nitrite production and did not influence the midintestinal motility. Our findings indicate that NO is involved in the neural transmission to intestinal muscles of gastropods, but enteric release of NO is blocked during dormancy. The decreased NO synthesis is possibly due to an as yet undefined mechanism, by which the l-arginine/NO conversion ability of NOS could temporarily be inhibited in the long-term resting period of H. lucorum.T. Röszer and Zs. Czimmerer contributed equally to this work as lead authors. This research was supported by OTKA grant no. T42762 (G.B.) and PRCH Student Science Foundation grants 2000, 2002 (T.R.) and 2003 (Zs. Cz). The study is dedicated to Borbála Vecsei-Czimmerer, Elemér Czimmerer, Ágnes M. Fodor-Röszer and József S. Röszer. 相似文献
2.
Gangping Hao Xihua Du Faxing Zhao Renjiu Shi Jianmei Wang 《Plant Cell, Tissue and Organ Culture》2009,97(2):175-185
The role of nitric oxide (NO) in UV-B-induced secondary metabolite accumulation in Ginkgo biloba callus was investigated. Overall, UV-B irradiation induced multiple biological responses in callus of G. biloba, including increased both NO production and nitric oxide synthase (NOS) activity, and subsequent activation of phenylalanine
ammonium lyase (PAL) and synthesis of flavonoids. Application of NO via the donor sodium nitroprusside (SNP) enhanced UV-B-induced
PAL activity and increased accumulation of flavonoids in G. biloba callus. Both, the NOS inhibitor l-NAME (N (G)-nitro-l-arginine methyl ester) and the NO scavenger c-PTIO (2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide) reduced the
production of NO. Moreover, UV-B-induced increase of PAL activity and flavonoid accumulation were suppressed by l-NAME and c-PTIO. These findings suggested a causal relationship between NO release and both PAL activity and flavonoid accumulation
under UV-B irradiation. In addition, it also indicated that NO, produced via NOS-like activity in ginkgo callus subjected
to UV-B irradiation, might act as an essential signaling molecule for triggering the activation of PAL and synthesis of flavonoids.
Additionally, a guanylyl cyclase inhibitor 6-anilino-5,8-quinolinequinone (LY-83583) prevented both UV-B- and SNP-induced
enhancement of PAL activation and flavonoid biosynthesis thus suggesting that the NO function was mediated by cyclic guanosine
5’-monophosphate. However, these effects of c-PTIO, l-NAME, and LY-83583 were partial, thus suggesting that there were NO-independent pathways in UV-B signaling networks.
Gangping Hao and Xihua Du are contributed equally to this article. 相似文献
3.
Brief limb ischemia was reported to protect neurons against injury induced by subsequent cerebral ischemia-reperfusion, and
this phenomenon is known as limb ischemic preconditioning (LIP). To explore the role of nitric oxide (NO) in neuroprotection
of LIP in rats, we observed changes in the content of nitric oxide (NO) and activity of NO synthase (NOS) in the serum and
CA1 hippocampus of rats after transient limb ischemic preconditioning (LIP), and the influence of NG-nitro-l-arginine methylester (l-NAME), a NOS inhibitor, on the neuroprotection of LIP against cerebral ischemia-reperfusion injury. Results showed that NO
content and NOS activity in serum increased significantly after LIP compared with the sham group. The increase showed a double
peak pattern, in which the first one appeared at time 0 (immediate time point) and the second one appeared at 48 h after the
LIP (P < 0.01). The NO content and NOS activity in the CA1 hippocampus in LIP group showed similar change pattern with the changes
in the serum, except for the first peak of up-regulation of NO content and NOS activity appeared at 6 h after LIP. Pretreatment
with l-NAME before LIP blocked the neuroprotection of LIP against subsequent cerebral ischemic insult. The blocking effect of l-NAME was abolished with pretreatment of l-Arg. These findings indicated that NO may be associated with the tolerance of pyramidal cells in the CA1 hippocampus to ischemia
induced by LIP in rats. 相似文献
4.
The present study was to test the hypothesis that 11,12-epoxyeicosatrienoic acid (11,12-EET), a metabolic product of arachidonic
acid by cytochrome P450 epoxygenase, regulates nitric oxide (NO) generation of the l-arginine/NO synthase (NOS) pathway in human platelets. Human platelets were incubated in the presence or absence of different
concentrations of 11,12-EET for 2 h at 37°C, followed by measurements of activities of the l-arginine/NOS pathway. Incubation with 11,12-EET increased the platelet NOS activity, nitrite production, cGMP content, and
the platelet uptake of l-[3H]arginine in a concentration-dependent manner. In addition, 11,12-EET attenuated intracellular free Ca2+ accumulation stimulated by collagen, which was at least partly mediated by EET-activated l-arginine/NOS pathway. It is suggested that 11,12-EET regulates platelet function through up-regulating the activity of the
l-arginine/NOS/NO pathway. 相似文献
5.
Cascade transduction and production of the light-nitric oxide signal from shoots to roots in maize seedlings exposed to enhanced UV-B radiation 总被引:1,自引:0,他引:1
The biomasses, rate of apparent nitric oxide (NO)-release, nitric oxide synthase (NOS) activity as well as β-d-endo and exo-glucanase activity of the cell wall were analyzed and determined in the roots of maize seedlings. It was found
that rhizospheric treatments of 2-phenyl-4,4,5,5-tetramethlimida-zoline-l-oxyl-3-oxide (PTIO), a NO scavenger, and radiation
of enhanced ultraviolet-B (UV-B) to aerial parts of the seedling markedly inhibited the rate of NO release in roots, raised
the activity of β-d-endo and exo-glucanase, and increased the biomasses of roots. The patent inhibitor, N-nitro-l-arginine (LNNA), of NOS was unable to inhibit NOS activity and NO generation. Inversely, reactive oxygen species (ROS) eliminator,
N-acetyl-cysteine (NAC), stimulated the rate of NO release. There is no relationship between NOS activity and the rate of NO
release. The latter showed a positive correlation with nitrate reductase (NR) activity, whereas it showed a negative correlation
with the bio-masses and the activity of β-d-endo and exo-glucanase. All results implicated that NO was a by-product generated by NR catalysis, whereas NR activity was
sensitively repressed by the systemic signal network (involved in ROS) induced by enhanced UV-B. It indicated that the downstream
signal molecule of enhanced UV-B light is probably ROS which decreased NO generation through inhibiting NR activity. The endogenous
NO generated by NR catalysis is perhaps such a messenger for restraining β-d-endo and exo-glucanase activity that the root growth was retarded. 相似文献
6.
Genestra M Souza WJ Guedes-Silva D Machado GM Cysne-Finkelstein L Bezerra RJ Monteiro F Leon LL 《Archives of microbiology》2006,185(5):348-354
Due to the diversity of its physiological and pathophysiological functions and general ubiquity, the study of nitric oxide (NO) has become of great interest. In this work, it was demonstrated that Leishmania amazonensis promastigotes produces NO, a free radical synthesized from l-arginine by nitric oxide synthase (NOS). A soluble NOS was purified from L. amazonensis promastigotes by affinity chromatography (2′, 5′-ADP-agarose) and on SDS-PAGE the enzyme migrates as a single protein band of 116.2 (±6) kDa. Furthermore, the presence of a constitutive NOS was detected through indirect immunofluorescence using anti-cNOS and in NADPH consumption assays. The present work show that NO production, detected as nitrite in culture supernatant, is prominent in promastigotes preparations with high number of metacyclic forms, suggesting an association with the differentiation and the infectivity of the parasite. 相似文献
7.
Despite evidence which supports a neurotransmitter-like role for nitric oxide (NO) in the CNS, relatively little is known regarding mechanisms which control NO formation within CNS neurons. In this study, isolated nerve endings (synaptosomes) from rat cerebral cortex were used to ascertain whether NO can autoregulate its own formation within neurons through feedback inhibition of the NO biosynthetic enzyme nitric oxide synthase (NOS). Under the conditions described here, N-nitro-l-arginine methyl ester-sensitive conversion ofl-[3H]arginine intol-[3H]citrulline (i.e., NOS activity) was found to be highly calcium-dependent and strongly inhibited (up to 60 percent) by NO donors, including sodium nitroprusside, hydroxylamine and nitroglycerin. The inhibitory effect of sodium nitroprusside was concentration-dependent (IC50100 M) and prevented by the NO scavenger oxyhemoglobin.l-Citrulline, the other major end-product from NOS, had no apparent effect on synaptosomal NOS activity. Taken together, these results indicate that neuronal NOS can be inhibited by NO released from exogenous donors and, therefore, may be subject to end-product feedback inhibition by NO that is formed locally within neurons or released from proximal cells. 相似文献
8.
Yamamoto Y Katsumata O Furuyama S Sugiya H 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2004,174(8):593-599
Nitric oxide (NO) plays an important role as an intra- and intercellular signaling molecule in mammalian tissues. In the submandibular gland, NO has been suggested to be involved in the regulation of secretion and in blood flow. NO is produced by activation of NO synthase (NOS). Here, we have investigated the regulation of NOS activity in the rabbit submandibular gland. NOS activity was detected in both the cytosolic and membrane fractions. Characteristics of NOS in the cytosolic and partially purified membrane fractions, such as Km values for l-arginine and EC50 values for calmodulin and Ca2+, were similar. A protein band that cross-reacted with anti-nNOS antibody was detected in both the cytosolic and membrane fractions. The membrane-fraction NOS activity increased 1.82-fold with treatment of Triton X-100, but the cytosolic-fraction NOS activity did not. The NOS activity was inhibited by phosphatidic acid (PA) and phosphatidylinositol 4,5-bisphosphate (PIP2). The inhibitory effects of phospholipids on the NOS activity were relieved by an increase in Ca2+ concentrations. These results suggest that the Ca2+- and calmodulin-regulating enzyme nNOS occurs in cytosolic and membrane fractions, and PA and PIP2 regulate the NOS activity in the membrane site by regulating the effect of Ca2+ in the rabbit submandibular gland.Communicated by I.D. Hume 相似文献
9.
Jennings BL Blake RE Joss JM Donald JA 《Comparative biochemistry and physiology. Part A, Molecular & integrative physiology》2008,151(4):590-595
The presence of nitric oxide synthase (NOS) and role of nitric oxide (NO) in vascular regulation was investigated in the Australian lungfish, Neoceratodus forsteri. No evidence was found for NOS in the endothelium of large and small blood vessels following processing for NADPH-diaphorase histochemistry. However, both NADPH-diaphorase histochemistry and neural NOS immunohistochemistry demonstrated a sparse network of nitrergic nerves in the dorsal aorta, hepatic artery, and branchial arteries, but there were no nitrergic nerves in small blood vessels in tissues. In contrast, nitrergic nerves were found in non-vascular tissues of the lung, gut and kidney. Dual-wire myography was used to determine if NO signalling occurred in the branchial artery of N. forsteri. Both SNP and SIN-1 had no effect on the pre-constricted branchial artery, but the particulate guanylyl cyclase (GC) activator, C-type natriuretic peptide, always caused vasodilation. Nicotine mediated a dilation that was not inhibited by the soluble GC inhibitor, ODQ, or the NOS inhibitor, L-NNA, but was blocked by the cyclooxygenase inhibitor, indomethacin. These data suggest that NO control of the branchial artery is lacking, but that prostaglandins could be endothelial relaxing factors in the vasculature of lungfish. 相似文献
10.
Chen YS Chen KH Liu CC Lee CT Yang CH Chuang KC Lin CR 《Journal of biomedical science》2007,14(5):629-636
The present study was undertaken to elucidate the mechanism of intra-arterial propofol-induced vascular permeability change
resulting in tissue edema. The mechanism of propofol-induced hyperpermeability was examined in a rat femoral artery injection
model. Vascular permeability was determined by measuring the Evans blue content of the dorsal skin of the infused limb at
15, 30, 45 and 60 min after propofol injection. The total content of the tight junction proteins occludin, ZO-1 and claudin-5
under experimental conditions was also determined by western blotting. Intra-arterial injection with propofol resulted in
a marked dose-dependent increase in vascular permeability of the rat hindpaw. Pretreatment with 10 mg/kg of N-nitro-l-arginine methyl ester (l-NAME) but not aminoguanidine significantly inhibited the change in vascular permeability after challenge with propofol. Pretreatment
with l-arginine and nitroprusside increased the propofol-induced permeability change. Intra-arterial injection of propofol significantly
increased occludin phosphorylation after 15 min, which was consistent with the time profile of the vascular permeability change.
l-NAME partially reversed the change in occludin phosphorylation, whereas aminoguanidine had no effect compared with that in
the controls. Our observations indicate that nitric oxide (NO) is an important mediator in the induction of vascular permeability
induced by propofol. Occludin phosphorylation is a determining factor in the vascular permeability change induced by propofol.
NO synthase (NOS) inhibitors might be useful in the treatment of accidental intra-arterial injection of propofol, in the reduction
of any adverse effects. 相似文献
11.
Isao Yokoi Yukiko Namba Hideaki Kabuto Kazunori Inada Motoyuki Iida Akitane Mori Norio Ogawa 《Neurochemical research》1996,21(10):1187-1192
Since nitric oxide (NO) is synthesized by nitric oxide synthase (NOS) froml-arginine (Arg) which has an amidino group in its molecule, we, examined the effect of 29 kinds of Arg analogues on neuronal
NOS (nNOS) activity in the rat brain. None of the Arg analogues acted as a substrate for nNOS. Diamidinocystamine, hirudonine,
and guanethidine inhibited nNOS activity to 67.3%, 64.2% and 74.1%, respectively, but their inhibitory efficiency was lower
than NG-monomethyl-l-arginine (to 36.5%) which is a well known NOS inhibitor. Dimethylguanidine and N-benzoylguanidine also significantly inhibited
nNOS activity to 88.0% and 90.7%, respectively. Whereas almost all of the NOS inhibitors previously reported were synthesizdd
by substituting the amidino nitrogen of Arg, none of these new inhibitors were substituted at this position. Furthermore,
hirudonine, which is a naturally occurring compound, was thought to act as an agonist at polyamine binding site of the N-methyl-d-aspartate type of glutamate receptor complex. It is also interesting that guanethidine, an antihypertensive agent, inhibit
nNOS activity. These new drugs are useful for the investigation not only of the chemical nature of nNOS but also of the physiologic
function of NO. 相似文献
12.
When grown in the light and in a Tris-acetate phosphate medium, cells of Chlamydomonas reinhardtii Dang. can use the following l-amino acids as a sole nitrogen source: asparagine, glutamine, arginine, lysine, alanine, valine, leucine, isoleucine, serine, methionine, histidine, and phenylalanine, whereas, in the absence of acetate, the cells only used l-arginine. The utilization system in the acetate medium consisted of an extracellular deaminating activity induced by l-amino acids; it took between 10 to 30 h before the system appeared in cells previously grown with ammonium. This deaminase activity was nonspecific, required an organic carbon source for its de-novo synthesis, and was sensitive to high ammonium concentration and light deprivation.Abbreviations HPLC
high-performance liquid chromatography
- TAP
Tris-acetate-phosphate
This work was supported by a grant of the CAICYT, Spain. The secretarial assistance of C. Santos and I. Molina is gratefully acknowledged.To whom correspondence should be addressed. 相似文献
13.
Taste cells are specialized epithelial cells that respond to stimulation with release of neurotransmitters onto afferent nerves
that innervate taste buds. In analogy to neurotransmitter release in other cells, it is expected that neurotransmitter release
in taste cells is dependent on an increase in intracellular Ca2+ ([Ca2+]
i
). We have studied changes in [Ca2+]
i
elicited by the taste stimuli l- and d-arginine in isolated taste cells from the channel catfish (Ictalurus punctatus). In a sample of 119 cells, we found 15 cells responding to l-arginine, and 12 cells responding to d-arginine with an increase in [Ca2+]
i
. The response to l-arginine was inhibited by equimolar d-arginine in cells where d-arginine alone did not cause a change in [Ca2+]
i
, which is consistent with mediation of this response by a previously characterized l-arginine-gated nonspecific cation channel antagonized by d-arginine [31]. However, we also found that these taste stimuli elicited decreases in [Ca2+]
i
in substantial number of cells (6 for l-Arg, and 2 for d-Arg, n= 119). These observations suggest that stimulation of taste cells with sapid stimuli may result in simultaneous excitation
and inhibition of different taste cells within the taste bud, which could be involved in local processing of the taste signal.
Received: 25 May 1995/Revised: 29 September 1995 相似文献
14.
Sephashvili M Zhuravliova E Barbakadze T Khundadze M Narmania N Mikeladze DG 《Neurochemical research》2006,31(10):1205-1210
Homocysteine is a sulfur-containing, nonproteinogenic, neurotoxic amino acid biosynthesized during methyl cycles after demethylation of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) and subsequent hydrolysis of SAH into homocysteine and adenosine. Formed homocysteine is either catabolized into cystathionine (transsulfuration pathway) by cystathionine β-synthase, or remethylated into methionine (remethylation pathway) by methionine synthase. To demonstrate the specificity of Ras-elicited effects on the activity of methyl cycles, wild-type pheochromocytoma PC12, mutant oncogenic rasH gene (MVR) expressing PC12 pheochromocytoma and normal c-rasH stably transfected M-CR3B cells were incubated with the Nω-nitro-l-arginine methyl ester (l-NAME), and manumycin, (inhibitors of nitric oxide synthase and farnesyltransferase, respectively). We have found that l-NAME significantly changes the SAM/SAH ratio in both MCR and MVR cells. Moreover, these alterations have reciprocal character; in the MCR cells, the SAM/SAH ratio was raised, whereas in the MVR cells this ratio was decreased. We conclude that depletion of endogenous NO with l-NAME increased the production of SAH only in cells with mutated oncogenic RasH, possibly through enhancement of production of reactive oxygen species (ROS). Oxidative stress can increase cystathionine β-synthase activity that switches methyl cycles from remethylation into transsulfuration pathway to maintain the intracellular glutathione pool (essential for the redox-regulating capacity of cells) via an adaptive process. 相似文献
15.
Corinne Vander Wauven Alfred Jann Dieter Haas Thomas Leisinger Victor Stalon 《Archives of microbiology》1988,150(4):400-404
Most Pseudomonas aeruginosa PAO mutants which were unable to utilize l-arginine as the sole carbon and nitrogen source (aru mutants) under aerobic conditions were also affected in l-ornithine utilization. These aru mutants were impaired in one or several enzymes involved in the conversion of N2-succinylornithine to glutamate and succinate, indicating that the latter steps of the arginine succinyltransferase pathway can be used for ornithine catabolism. Addition of aminooxyacetate, an inhibitor of the N2-succinylornithine 5-aminotransferase, to resting cells of P. aeruginosa in ornithine medium led to the accumulation of N2-succinylornithine. In crude extracts of P. aeruginosa an ornithine succinyltransferase (l-ornithine:succinyl-CoA N2-succinyltransferase) activity could be detected. An aru mutant having reduced arginine succinyltransferase activity also had correspondingly low levels of ornithine succinyltransferase. Thus, in P. aeruginosa, these two activities might be due to the same enzyme, which initiates aerobic arginine and ornithine catabolism.Abbreviations OAT
ornithine 5-aminotransferase
- SOAT
N2-succinylornithine 5-aminotransferase
- Oru
ornithine utilization
- Aru
arginine utilization 相似文献
16.
Highly metastatic ras/myc-transformed serum-free mouse embryo (r/m HM-SFME-1) cells were injected subcutaneously to mice and the effects of Nω-nitro-l-arginine methyl ester (l-NAME) on the tumor progression and pulmonary metastasis were investigated. In addition, production of nitric oxide (NO), matrix
metalloproteinases (MMPs) and tumor necrosis factor-alpha (TNF-α) in the tumor cells and in a mouse macrophage-like cell line,
J774.1 cells, was analyzed. The increase in footpad thickness was significantly smaller in the mice which were fed the l-NAME containing water (4.24 ± 0.39 mg/day/mouse). The number of the tumor cells metastasized to the lungs was smaller in
the l-NAME treated mice, although statistical significance was not found. Co-treatment of r/m HM-SFME-1 cells with interferon-gamma (IFN-γ; 100 U/ml) and lipopolysaccharide (LPS; 0.5 μg/ml) significantly enhanced NO
production, and the presence of l-NAME at 1 mM significantly decreased this response. In r/m HM-SFME-1 cells, MMP-2 was undetectable and MMP-9 was also very little in the basal level, and both MMPs were unaffected
by the IFN-γ and/or LPS treatments, not to mention by the l-NAME treatment. In J774.1 cells, any treatment including LPS appeared to enhance MMP-9 production, however, this upregulation
was not inhibited by the additional presence of l-NAME. Production of TNF-α by J774.1 cells was markedly enhanced with LPS treatment, and this enhancement was significantly
reduced in the presence of l-NAME. These results indicate that the inhibitory effects of l-NAME on the tumor cell progression and pulmonary metastasis could be due to suppression of NO from tumor cells and TNF-α
from macrophages (Mol Cell Biochem, 2007).
Hideaki Yamaguchi and Yumi Kidachi contributed equally to this work. 相似文献
17.
Constitutive arginine-dependent nitric oxide synthase activity in different organs of pea seedlings during plant development 总被引:20,自引:0,他引:20
Corpas FJ Barroso JB Carreras A Valderrama R Palma JM León AM Sandalio LM del Río LA 《Planta》2006,224(2):246-254
Nitric oxide (NO) is an important signalling molecule in different animal and plant physiological processes. Little is known about its biological function in plants and on the enzymatic source or site of NO production during plant development. The endogenous NO production from l-arginine (NO synthase activity) was analyzed in leaves, stems and roots during plant development, using pea seedlings as a model. NOS activity was analyzed using a novel chemiluminescence-based assay which is more sensitive and specific than previous methods used in plant tissues. In parallel, NO accumulation was analyzed by confocal laser scanning microscopy using as fluorescent probes either DAF-2 DA or DAF-FM DA. A strong increase in NOS activity was detected in stems after 11 days growth, coinciding with the maximum stem elongation. The arginine-dependent NOS activity was constitutive and sensitive to aminoguanidine, a well-known irreversible inhibitor of animal NOS, and this NOS activity was differentially modulated depending on the plant organ and seedling developmental stage. In all tissues studied, NO was localized mainly in the vascular tissue (xylem) and epidermal cells and in root hairs. These loci of NO generation and accumulation suggest novel functions for NO in these cell types. 相似文献
18.
Hong E Larios F Gómez-Viquez NL Huang F Bravo G 《Journal of physiology and biochemistry》2011,67(3):427-435
The contribution of α-adrenoceptors and nitric oxide (NO) on the alterations of sympathetically mediated cardiovascular responses
after acute (AcH) and chronic (ChH) hypertension was evaluated in pithed aortic coarcted hypertensive rats. Pressor and tachycardia
response produced by electrical stimulation of preganglionic sympathetic fibers or exogenous noradrenaline (NA) were recorded
in the absence and presence of prazosin (α1-antagonist), rauwolscine (α2-antagonist), or N
G-nitro-l-arginine methyl ester (l-NAME; an inhibitor of NO synthase). Compared with age-matched sham-operated rats (Nt), the pressor response produced by electrical
stimulation or NA was smaller in AcH rats and larger in ChH rats. Prazosin caused a decrease of pressor response elicited
by electrical stimulation or NA in all groups. However, this effect was higher in ChH. Rauwolscine produced a similar increase
of sympathetically mediated pressor response in Nt and AcH rats. Nevertheless, this antagonist did not affect the sympathetically
mediated pressor response in ChH rats. In addition, rauwolscine did not affect the NA-induced pressor response in all groups.
The pressor response elicited by l-NAME was larger in all groups compared without l-NAME and in presence of l-arginine. Moreover, l-NAME in the presence of NA increased sympathetically mediated pressor response is in all groups, compared without it or in
the presence of l-arginine. Compared with Nt, basally produced NO in aortic rings was increased in AcH but decreased in ChH. Collectively,
our data suggest that decreased cardiovascular reactivity in AcH is due to an increase in basally produced NO. In ChH, enhanced
cardiovascular response appears to be associated with a decrease in produced NO and an increase in released NA from sympathetic
nerves. 相似文献
19.
R. C. Srivastava A. Farookh Nihal Ahmad Minakshi Misra S. K. Hasan M. M. Husain 《Biometals》1996,9(2):139-142
Cisplatin treatment of rats results into a significant increase in the activity of Ca2+-independent nitric oxide synthase (NOS) in kidneys and liver. Significant enhancement of lipid peroxidation in gastric mucosa, kidneys and liver was also observed. The administration of N
G-nitro-l-arginine methyl ester, an inhibitor of NOS, markedly reduced renal and gastrointestinal toxicity, and also decreased the content of blood urea nitrogen, serum creatinine, and incidence of diarrhoea along with a significant inhibition in lipid peroxidation in the target organs. The present report, while demonstrating the beneficial effect of the blockade of NO pathways during cisplatin chemotherapy, may be helpful in developing strategies for combating some of the toxic side-effects of the drug.Present address: Department of Dermatology, Case Western Reserve University, Cleveland. OH 44106. USA. 相似文献
20.
Co-localization of nitric oxide synthase immunoreactivity and NADPH diaphorase staining in neurons of the guinea-pig intestine 总被引:1,自引:0,他引:1
H. M. Young J. B. Furness C. W. R. Shuttleworth D. S. Bredt S. H. Snyder 《Histochemistry and cell biology》1992,97(4):375-378
Summary Neuronal nitric oxide synthase (NOS), an enzyme capable of synthesizing nitric oxide, appears to be identical to neuronal NADPH diaphorase. The correlation was examined between NOS immunoreactivity and NADPH diaphorase staining in neurons of the ileum and colon of the guinea-pig. There was a one-to-one correlation between NOS immunoreactivity and NADPH diaphorase staining in all neurons examined; even the relative staining intensities obtained were similar with each technique. To determine whether pharmacological methods could be employed to demonstrate that NADPH diaphorase staining was due to the presence of NOS, tissue was pre-treated with NG-nitro-l-arginine, a NOS inhibitor, or l-arginine, a natural substrate of NOS. In these experiments on unfixed tissue, it was necessary to use dimethyl thiazolyl tetrazolium instead of nitroblue tetrazolium as the substrate for the NADPH diaphorase histochemical reaction. Neither treatment caused a significant decrease in the level of NADPH diaphorase staining, implying that arginine and NADPH interact at different sites on the enzyme. 相似文献