Wyniki wyszukiwania - AGRO

1

Cerivastatin potentiates nitric oxide release and eNOS expression through inhibition of isoprenoids synthesis

100%

Kalinowski L., Dobrucki I. T., Malinski T.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Endothelium dysfunction, which is often defined as a decrease in NO bioavailability, is one of the earliest manifestations of endothelium-impaired function disorders, including atherosclerosis. Although improvement in NO bioavailability has been attributed to the lowering of serum cholesterol levels, recent studies suggest that HMG-CoA reductase inhibitors, statins, may have direct effects on NO bioavailability by little known mechanisms that are independent of serum cholesterol levels. The long-term effect of cerivastatin on NO release from endothelial cells was determined by using highly sensitive electrochemical microsensors and was correlated with endothelial NO synthase (eNOS) levels. To explore whether changes in isoprenoid synthesis affect NO bioavailability and eNOS expression, human endothelial cells were treated with cerivastatin, L-mevalonate (MVA; 1.5 mmol/L), geranylgeranylpyrophosphate (GGPP; 1 mg/mL) and farnesylpyrophosphate (FPP; 1 mg/mL). Cerivastatin increased spontaneous (by 53% ±6) and an eNOS-stimulated NO release (by 41 ±6% for calcium ionophore and by 47±5% acetylcholine) as well as eNOS expression (by 118 ±6%) in the same concentration-range. Cerivastatin- dependent increase in both NO release and eNOS expression was revealed after ~4 h of exposure reaching the maximum after ~10 h. Co-treatment with MVA or GGPP, but not FPP or LDL, reversed the effects of cerivastatin. These findings indicate that the long-term effect of cerivastatin resulting in enhanced NO bioavailabilty in endothelial cell is, at least in part, due to up-regulation of eNOS by blocking isoprenoids synthesis.

2

The effect of potassium channel blockers on the relaxant response of human intrauterine arteries to exogenous nitric oxide

100%

Kostrzewska A.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

3

Nitric oxide as a signalling molecule

100%

Wrzosek A.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr Suppl.

4

Endogenous inhibitors of no synthase

100%

MacAllister R. J., Vallance P.

Journal of Physiology and Pharmacology. Supplement

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1993

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tom 44

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nr 2

5

The effect of NO on metabolism of acetylcholine in the brain

100%

Szutowicz A., Tomaszewicz M., Jankowska A., Bielarczyk H.

Polish Journal of Environmental Studies

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1998

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tom 07

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nr 6

6

Nitric oxide effect on the hemoglobin-oxygen affinity

100%

Stepuro T. L., Zinchuk V. V.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 1

The biological roles of nitric oxide (NO)-hemoglobin (Hb) derivatives are obscure. It is proposed that NO can function as an allosteric regulator of hemoglobin oxygen-binding properties. We aimed to estimate the effects of NO donors and NO-synthase substrate (L-arginine) on hemoglobin-oxygen affinity (HOA) in experiments in vitro with the various ratios between NO formed and Hb and various oxygen pressures. HOA index (p50), blood pH, plasma and red blood cell (RBC) concentrations of nitrite/nitrate and methemoglobin amounts were measured after the experiments. In our experiments, blood incubation with NO donors (glyceryltrinitrate, molsidomine, sodium nitroprusside, S-nitrosocysteine) or NO-synthase substrate (L-arginine) did not change HOA even at NO:Hb ratio of 1:1. At the same time our results showed that oxygenated blood incubation with S-nitrosocysteine induced an oxyhemoglobin dissociation curve shift leftwards. This indicates a leading role of met-Hb in a modification of Hb oxygen-binding properties. However other NO-modified forms of hemoglobin (S-nitroso- and nitrosylhemoglobin) also may be involved in the regulation of HOA. The results obtained indicate that nitric oxide can be the allosteric effector of hemoglobin, increasing or decreasing its oxygen affinity - possibly, through the generation of different NO-Hb derivatives.

7

The role of endogenous nitric oxide in inhibition of ischemia-reperfusion-induced cardiomyocyte apoptosis

88%

Czarnowska E., Kurzelewski M., Beresewicz A., Karczmarewicz E.

Folia Histochemica et Cytobiologica

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2001

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tom 39

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nr 2

8

INOS expression and NO production by neutrophils in cancer patients

88%

Jablonska E., Puzewska W., Marcinczyk M., Grabowska Z., Jablonski J.

Archivum Immunologiae et Therapiae Experimentalis

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2005

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tom 53

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nr 2

9

A modified method allows for correlation between NADH-diaphorase histochemistry and immunohistochemistry for the demonstration of neuronal nitric oxide synthase [ nNOS ]

88%

Grozdanovic Z., Nakos G., Mayer B., Gossrau R.

Folia Histochemica et Cytobiologica

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1995

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tom 33

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nr 1

10

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Nitric oxide inhibits the myoelectric activity of the small intestine in dogs

88%

Maczka M., Thor P., Lorens K., Konturek S. J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 1

11

The overproduction of nitric oxide associated with neutrophilic predominance is relevant to airway mycotic infections in asthmatics undergoing prolonged glucocorticoid treatment

88%

Cembrzynska-Nowak M., Liebhart J., Bienkowska-Haba M., Liebhart E., Kulczak A., Siemieniec I., Dobek R., Dor A., Barg W., Panaszek B.

Cellular and Molecular Biology Letters

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2005

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tom 10

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nr 4

12

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

88%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 2

Nitric oxide (NO) is a major signaling molecule and biological mediator of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the role of NO formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS) in the stimulatory effect of nicotine on the HPA axis in rats under basal conditions. Also possible interaction of NOS systems with endogenous prostaglandins (PG) in that stimulation was assessed. NOS and cyclooxygenase inhibitors were administered i.p. 15 min prior to nicotine (2, 5 mg/kg i.p.). Plasma ACTH and serum corticosterone levels were measured 1 h after nicotine injection. NOS blockers given alone did not markedly affect the resting ACTH and corticosterone levels. L-NAME (2-10 mg/kg), a broad spectrum NOS inhibitor considerably and dose dependently enhanced the nicotine-induced ACTH and corticosterone secretion. L-NNA (2 mg/kg) and 7-nitroindazole (7-NI 20 mg/kg), neuronal NOS inhibitors in vivo also significantly augmented the nicotine-induced ACTH and corticosterone levels. L-arginine greately impaired the nicotine-induced hormone responses and reversed the L-NNA elicited enhancement of the nicotine-evoked ACTH and corticosterone response. In contrast to the constitutive eNOS and nNOS antagonists, an inducible NOS antagonist guanethidine (50-100 mg/kg i.p.) did not substantially affect the nicotine-elicited pituitary-adrenocortical responses. Indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase blocker abolished the L-NAME and L-NNA-induced enhancement of the nicotine-evoked ACTH and corticosterone response. These results indicate that NO is an inhibitory mediator in the HPA axis activity. Inhibition of its generation by eNOS and nNOS significantly enhances the nicotine-induced HPA response. Under basal conditions iNOS is not involved in the nicotine-induced ACTH and corticosterone secretion. Prostaglandins play an obligatory role in the response of HPA axis to systemic nicotine administration.

13

Control of the circulation by chemical mediators from the endothelium

88%

Vane J. R., Botting R. M.

Journal of Physiology and Pharmacology. Supplement

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1993

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tom 44

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nr 2

14

Role of prostaglandins and nitric oxide in the lipopolysaccharide-induced ACTH and corticosterone response

88%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

This study was designed to determine the role of endogenous prostaglandins (PG) and nitric oxide (NO) in the lipopolysaccharide (LPS)-induced ACTH and corticosterone secretion in conscious rats. LPS (0.5 and 1 mg/kg) given i.p. stimulated the hypothalamic-pituitary-adrenocortical (HPA) activity measured 2 h later. A non-selective cyclooxygenase inhibitor indomethacin (10 mg/kg i.p.), piroxicam (2 mg/kg i.p.), a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (2 mg/kg i.p.), a selective inhibitor of inducible cyclooxygenase (COX-2) given 30 min before LPS (1 mg/kg i.p.) significantly diminished both the LPS-induced ACTH and corticosterone secretion. COX-2 blocker was the most potent inhibitor of ACTH secretion (72.3%). Nw-nitro-L-arginine methyl ester (L-NAME 2 and 10 mg/kg i.p.), a non-selective nitric oxide synthase (NOS) blocker given 15 min before LPS did not substantially alter plasma ACTH and corticosterone levels 2 h later. Aminoguanidine (AG 100 mg/kg i.p.), a selective inducible nitric oxide synthase (iNOS) inhibitor, considerably enhanced ACTH and corticosterone secretion induced by a lower dose (0.5 mg/kg) of LPS and did not significantly alter this secretion after a larger dose (1 mg/kg) of LPS. L-NAME did not markedly affect the indomethacin-induced inhibition of ACTH and corticosterone response. By contrast, aminoguanidine abolished the indomethacin-induced reduction of ACTH and corticosterone secretion after LPS. These results indicate an opposite action of PG generated by cyclooxygenase and NO synthesized by iNOS in the LPS-induced HPA-response.

15

Physiological mediators in nonsteroidal anti-inflammatory drugs (NSAIDs)-induced impairment of gastric mucosal defense and adaptation. Focus on nitric oxide and lipoxins

88%

Brzozowski T., Konturek P. C., Pajdo R., Ptak-Belowska A., Kwiecien S., Pawlik M., Drozdowicz D., Sliwowski Z., Brzozowski B., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 2

Prostaglandins mediate various physiological aspects of mucosal defense and the suppression of prostaglandin synthesis in the stomach is a critical event in terms of the development of mucosal injury after NSAID administration. However, it has become clear that other mediators besides prostaglandins can similarly act to protect the stomach from injury. For instance, nitric oxide (NO) released from vascular epithelium, epithelial cells of gastrointestinal tract and sensory nerves can influence many of the same components of mucosal defense as do prostaglandins. Thus, administration of NO in a form of NO-donors exert protective influence on the stomach from the injury that usually occurs when mucosal prostaglandin levels are suppressed. The new class of NO releasing NSAIDs, including NO-aspirin, represent a very promising approach to reducing the toxicity of anti-inflammatory drugs. Lipoxins are another group of lipid mediators that can protect the stomach. Aspirin-triggered lipoxin synthesis, via COX-2, acts to reduce the severity of damage induced by this drug. Lipoxin analogues may prove to be useful for preventing mucosal injury and for modulating mucosal inflammation. Aspirin-triggered lipoxin also seems to play in important role in gastric adaptation during chronic aspirin administration. Suppression of COX-2 activity by selective COX-2 inhibitors abolishes the production of this endogenous gastroprotective substance and diminishes the gastric tolerability of NSAIDS and gastric adaptation to these drugs. This review was designed to give an updated overview on the physiological factors and experimental and clinical attempts that were used or may be used in the future as the therapeutic approach to counteract adverse effects in the stomach associated with NSAID ingestion.

16

Microcirculatory and motor effects of endogenous nitric oxide in the rat gut

88%

Pawlik W. W., Gustaw P., Thor P., Sendur R., Czarnobilski K., Hottenstein O. D., Konturek S. J.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 2

17

Synergistic antiplatelet action of nitric oxide [NO] with PGD2 and its metabolite PGJ2 - relevance for cerebral circulation?

88%

Rodrigues M., Fitscha P., Sinzinger H.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 4

18

An exonic G894T variant of endothelial nitric oxide synthase gene as a risk factor for ischemic stroke in North Indians

76%

Kaur K., Uppal A., Kaur A.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr 4

Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) enzyme is a critical regulator of cerebrovascular homeostasis. Genetic variability of G894T and intronic 4ab polymorphism in eNOS could affect the expression and activity of eNOS enzyme, modulating NO levels in endothelium. This results in endothelial dysfunction, which can contribute to the pathogenesis of ischemic stroke. The purpose of the study was to evaluate the association of eNOS genetic polymorphisms (G894T and 4ab) with the occurrence of ischemic stroke through various genetic models. Both polymorphisms were genotyped in 120 ischemic stroke patients diagnosed with MRI and other ancillary techniques and 101 control subjects free of neurological abnormalities, using PCR-RFLP technique and direct PCR respectively. The genotypes of both G894T and 4ab variants were found to be in Hardy Weinberg equilibrium for cases and controls. The significant variation was observed in the genotypic and allelic frequencies for G894T polymorphism between cases and controls, indicating the association of G894T variability with ischemic stroke. However, the difference between cases and controls was insignificant for eNOS 4ab polymorphism with regard to genotypic and allelic distribution. Except for recessive model, both dominant (GT/TT vs. GG) and co-dominant (TT vs. GT or GT vs. GG) models indicated nearly two-fold and 1.93 increased risk of ischemic stroke for G894T polymorphism, but none of them suggested the influence of eNOS 4ab polymorphism on ischemic stroke susceptibility. Haplotype analysis revealed the higher frequency of GT-4bb genotype combination in cases as compared to controls, but without significant difference. The study concluded that SNP G894T variant is associated with ischemic stroke and might contribute to ischemic stroke susceptibility in North Indians. However, this outcome needs to be confirmed by studies with large sample size.

19

Immunohistochemical evaluation of caspase 3 expression in rats' hepatocytes after L-arginine therapy

76%

Pedrycz A., Kot K., Olesinski I.

Bulletin of the Veterinary Institute in Puławy

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2010

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tom 54

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nr 1

101-103

The apoptotical effect of nitric oxide on effector apoptotical caspase 3 in rats' hepatocytes was examined. The experiment was performed on 16 white Wistar female rats divided into two equal groups. The rats from the experimental group received orally L-arginine in a dose of 40 mg/kg b.w. every other day for 2 weeks. The rats from the control group received orally 2 ml of distilled water in the same manner as the experimental group. All the rats were decapitated after 3 weeks of the experiment. After decapitation, specimens from the liver were collected, fixed in 10% formalin, and then embedded in paraffin blocks. Protein caspase 3 on slides was detected using the standard three-step immunohistochemical method. The quantitative evaluation of caspase 3 expression showed that the area occupied by positive caspase 3 reaction in the liver of the experimental group (128.11 µm²±96.54) was comparable to that in the control group (212.18 µm² ±1 16.59) (P=0.25). The dose of L-arginine used was similar to that applied in pregnant women treated for gestosis. The study shows that L-arginine as a donor of exogenous nitric oxide has no an apoptotic effect on rats' hepatocytes.

20

Exogenous nitric oxide inhibits shedding of ADAM17 substrates

76%

Bzowska M., Stalinska K., Mezyk-Kopec R., Wawro K., Duda K., Das S., Bereta J.

Acta Biochimica Polonica

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2009

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tom 56

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nr 2

325-335

Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report.

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