Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to investigate whether in vivo and in vitro erythropoietin (EPO) production is modulated by nitric oxide (NO) and cyclic guanosine 3',5'-monophosphate (cGMP). Serum levels of EPO in ex-hypoxic polycythemic mice were significantly increased after injections of 200 micrograms/kg sodium nitroprusside for 4 d. One injection of NG-nitro-L-arginine methyl ester (L-NAME) produced a significant dose-related decrease in serum levels of EPO in ex-hypoxic polycythemic mice in response to hypoxia. When EPO producing Hep3B cells were incubated in 1% O2 for 30 min, cGMP levels in the Hep3B cells were significantly elevated, compared with cells incubated in 20% O2. The elevation of cGMP by hypoxia was inhibited by L-NAME (100 microM). Sodium nitroprusside (10 and 100 microM) and NO (2 microM) also significantly increased cGMP levels in Hep3B cells. L-NAME, LY 83583 (6-Anilino-5,8-quinolinedione, a soluble guanylate cyclase inhibitor), and Rp-8-Bromo-cGMPS (Rp-8-Bromo-guanosine 3',5'-cyclic monophosphothioate, a cGMP-dependent protein kinase inhibitor) significantly inhibited the hypoxia-induced increase in medium levels of EPO in Hep3B cells. 8-Bromo-cGMPS produced a dose-dependent decrease in EPO messenger RNA levels in Hep3B cells in response to hypoxia. 8-Bromo-cGMP (10(-3) M) produced significant increases in medium levels of EPO in Hep3B cell cultures incubated under normoxic conditions, which was enhanced by the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (0.2 mM). These results suggest that NO and cGMP may interact in modulating hypoxic stimulation of EPO production.
J Clin Invest 1993 Sep
PMID:Interaction of nitric oxide and cyclic guanosine 3',5'-monophosphate in erythropoietin production. 839 29

A three month visual training programme was conducted at the CAR of Sant Cugat (Olympic Training Center). Eleven members of 'The Catalan Government Special Intervention Squad' were used in a clinical trial. Pre-test and post-test results were obtained for pistol shooting, visual function, and psychological and physical states. Statistical analysis indicated significant gains in visual function and pistol shooting scores after the programme, while psychological (anxiety) and physical condition remained the same. Some conclusive statements can be made with regard to the relation of visual function improvement and shooting performance increment, after analysing the data. This improvement is evident in statistically significant post-test gains in the following variables: 'phoria at distance, recovery points in fusional reserves at distance, analytical amplitude, negative relative accommodation, saccadic fixations, and accommodative facility at distance and at near. The rest of the controlled visual variables also showed clinical improvement.
Ophthalmic Physiol Opt 1995 Sep
PMID:Visual training programme applied to precision shooting. 852 86

The effects of i.p. administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methylester (L-NAME) and its inactive isomer, D-NAME, were tested in two nociceptive paradigms in the rat. In the first paradigm, rats were lightly anaesthetized with a mixture of chloral hydrate (120 mg/kg, i.p.) and sodium pentobarbital (20 mg/kg, i.p.). Tail flick reaction times were monitored and thermal hyperalgesia was induced by immersion of the tail in hot water at 55 degrees C for 1.5 min. In the groups of rats pretreated with saline (n = 5), 100 mg/kg D-NAME (n = 6), 10 (n = 5) or 25 (n = 6) mg/kg L-NAME, this thermal injury induced a transient reduction in the reaction time that was 54-59% of the baseline value. However, in the groups of rats pretreated with 50 (n = 6) or 100 (n = 7) mg/kg L-NAME the reaction times were 73.9 +/- 2.7% (P < 0.05) and 102.3 +/- 0.9% (P < 0.001) of the baseline values respectively, indicating a block of the hyperalgesic responses seen in the other groups. As this hyperalgesia has been reported to be blocked by NK-1 receptor antagonists, it is suggested that it is due to the action of endogenous substance P. In the second paradigm, tail flick responses were monitored in the awake rat and thermal hyperalgesia was induced by intrathecal administration of substance P (6.5 nmol) via a chronically implanted catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
Eur J Neurosci 1995 Sep 01
PMID:Implication of a nitric oxide synthase mechanism in the action of substance P: L-NAME blocks thermal hyperalgesia induced by endogenous and exogenous substance P in the rat. 852 67

In non-allergic subjects, histamine induced a reduction of minimal nasal cross-sectional area (Amin) and an increase in albumin release into nasal lavage. The effect of histamine on albumin release was inhibited by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), 1 mumol but not by D-NAME, 1 mumol. L-NAME, 1 and 10 mumol, did not inhibit the histamine-induced reduction of Amin. In subjects allergic to grass pollen, antigen challenge induced a reduction in Amin that was not changed by pretreatment with L-NAME, and an increase in albumin release that was inhibited by L-NAME, 1 mumol. The data support a role for nitric oxide in mediating plasma extravasation in the nose induced by antigen challenge or histamine.
Br J Pharmacol 1995 Sep
PMID:Reduction by NG-nitro-L-arginine methyl ester (L-NAME) of antigen-induced nasal airway plasma extravasation in human subjects in vivo. 852 50

Changes in the populations of neurotransmitter receptors involved in the control of intestinal smooth muscle function have been associated with the altered motility of the inflamed gut. Thus, trinitrobenzenesulphonic acid (TNBS)-induced gut inflammation is accompanied by an increase in alpha- and a decrease in beta-adrenoceptor numbers in guinea pig small intestine. In the present study, we investigated the effects of anti-inflammatory compounds (cyclooxygenase inhibitor indomethacin, lipooxygenase inhibitor MK-886, nitric oxide synthase inhibitor NG-nitro-L-arginine methylester (L-NAME), mast cell stabilizer doxantrazole) on TNBS-induced adrenoceptor changes. Smooth muscle adrenoceptor populations, labelled by subtype-specific radioligands 6 days after TNBS, were significantly different from those of sham-treated controls: alpha 1- and alpha 2-adrenoceptor numbers increased by more than 50%, while beta-adrenoceptor numbers decreased by more than 50%. These changes, associated with severe inflammation as assessed histologically and by myeloperoxidase assay, were prevented by doxantrazole or L-NAME, and only partly by MK-886. In contrast, indomethacin did not prevent these changes. It appears then that: (a) mast cell mediators, nitric oxide and leukotrienes are likely to contribute to TNBS-induced changes in adrenoceptor populations in the guinea pig inflamed intestine; (b) there is no evidence for prostanoid involvement in this process. It was suggested that changes in smooth muscle adrenoceptor populations may be an important mechanism by which gut inflammation alters intestinal motility.
Neurogastroenterol Motil 1995 Sep
PMID:Evidence for mast cell, leukotriene and nitric oxide involvement in the regulation of the adrenoceptor number of inflamed small intestine in guinea pigs. 853 63

Biochemical signaling determines the specific action of vasomediators in the control of microvascular permeability and tone. We tested the hypothesis that nitric oxide (NO) synthesis is involved in the biochemical signaling pathway of platelet activating factor (PAF). The cheek pouch of anesthetized male Syrian hamsters was used as a microvascular model. Vessel diameter [expressed as the ratio of the experimental to the control (e/c) diameter, with control diameter normalized to 1] and extravasation of FITC-dextran 150 by integrated optical intensity (IOI) were determined using intravital fluorescent microscopy and computer-assisted digital image analysis. N-Nitro-L-arginine methyl ester (L-NAME) at 10(-5) and 10(-6) M and N-nitro-L-mono-methyl arginine (L-NMMA) at 10(-4) and 10(-5) M were used as inhibitors of NO synthase (NOS). Acetylcholine (ACh) and bradykinin were used as indirect indices of NOS activation. L-NAME and L-NMMA attenuated both ACh and bradykinin vasodilatory effects as well as the bradykinin-induced increase in vascular permeability. Topical PAF (10(-7) M) caused vasoconstriction (mean +/- SEM e/c ratio = 0.3 +/- 0.1) and increased IOI from a normalized baseline of 0 to 67.4 +/- 12.8. Topical administration of L-NAME produced differential effects on the series-arranged arterioles but had no effect on postcapillary venular permeability. L-NMMA did not influence the basal arteriolar diameter, but at 10(-5) M it caused a small increase in permeability (IOI = 14.3 +/- 4.2). In the presence of NOS inhibitors, PAF caused a reduced arteriolar constriction (e/c ratio = 0.6 +/- 0.1) relative to PAF alone. Both NOS inhibitors reduced the PAF-stimulated increase in vasopermeability. At 10(-5) M L-NMMA, the PAF-stimulated IOI mean value was 26.1 +/- 5.2, while at 10(-4) M L-NMMA the PAF-stimulated IOI was 15.2 +/- 2.6 compared to 10(-7) M PAF (67.4 +/- 12.8). These results support our hypothesis that NO synthesis is a step in the biochemical signaling pathway of the postcapillary cellular responses to PAF.
Microvasc Res 1995 Sep
PMID:Platelet activating factor modulates microvascular permeability through nitric oxide synthesis. 853 2

The effect of pituitary adenylate cyclase activating peptide (PACAP 1-27) was examined on epithelium-intact and -denuded guinea-pig tracheal strips (GPT) and compared to vasoactive intestinal peptide (VIP) and salbutamol. PACAP (10(-11)-10(-8) moles) induced dose-dependent relaxations of the basal tone of both epithelium-intact and -denuded GPT. PACAP was approximately three times less potent than either VIP or salbutamol in relaxing epithelium-intact GPT. The relaxant effects of both peptides and salbutamol were markedly attenuated following removal of the epithelial layer. L-NAME (10(-4) M), a nitric oxide synthase inhibitor, did not affect the responses induced by either PACAP or VIP demonstrating that the relaxant effect is independent of nitric oxide synthesis. Phosphoramidon (5 x 10(-6) M) potentiated the relaxant responses of epithelium-intact GPT to both PACAP and VIP but did not affect the responses of epithelium-denuded GPT. PACAP and VIP also induced relaxations of the guinea-pig upper bronchus. In addition, PACAP (10(-6) M), as well as VIP, significantly inhibited the release of TxB2 induced by LTD4 (10(-7) M) from chopped guinea-pig lung suggesting that this newly isolated peptide, which has 68% homology with VIP, may possess anti-inflammatory action in the lung.
Neuropeptides 1995 Sep
PMID:Relaxant effects of pituitary adenylate cyclase activating polypeptide (PACAP) on epithelium-intact and -denuded guinea-pig trachea: a comparison with vasoactive intestinal peptide (VIP). 853 72

Circadian rhythms in mammals are entrained to the environmental light cycle by daily adjustments in the phase of the circadian pacemaker located in the suprachiasmatic nuclei (SCN) of the hypothalamus. Brief exposure of hamsters maintained under constant darkness to ambient light during subjective nighttime produces both phase shifts of the circadian activity rhythm and characteristic patterns of c-fos protein (Fos) immunoreactivity in the SCN. In this study, we demonstrate that light-induced phase shifts of the circadian activity rhythm are blocked by intracerebroventricular (i.c.v.) injection of the competitive nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), but not by the inactive isomer, D-NAME. The effects of L-NAME are reversible and dose-related, and are countered by co-injection of arginine, the natural substrate for NOS. While effects on behavioral rhythms are pronounced, similar treatment does not alter the pattern of light-induced Fos immunoreactivity in the SCN. These results suggest that nitric oxide is a component of the signal transduction pathway that communicates photic information to the SCN circadian pacemaker, and that nitric oxide production is either independent of, or downstream from, pathways involved in induction of c-fos expression.
Brain Res 1995 Sep 18
PMID:Nitric oxide synthase inhibitor blocks light-induced phase shifts of the circadian activity rhythm, but not c-fos expression in the suprachiasmatic nucleus of the Syrian hamster. 854 97

The role of nitric oxide (NO) as an inflammatory mediator in the mechanism of increased microvascular permeability was examined in a guinea pig model of allergic conjunctivitis. Topical challenge with antigen, compound 48/80, histamine or platelet activating factor (PAF) resulted in a marked increase of the conjunctival vascular permeability. Vascular permeability was determined by measuring the albumin content in the lavage fluid of the challenged eyes after 30 min. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) eyedrops caused a significant inhibition of the clinical score and the vascular permeability after challenge with either antigen, histamine or PAF. Aminoguanidine prophylaxis also resulted in a significant inhibition of both the clinical score and vascular permeability in response to all the used provocative agents except PAF. Our observations indicate that NO is an important factor in the induction of the vascular permeability provoked by histamine but seems to play no role in the mechanism by which PAF exerts increased vascular permeability in the conjunctiva.
Eur J Pharmacol 1995 Sep 15
PMID:Nitric oxide induces vascular permeability changes in the guinea pig conjunctiva. 854 37

In isolated pancreative beta cells from rats the insulin secretory response to glucose is amplified by L-arginine. Since this effect is inhibited by NO synthesis inhibitors, and since L-arginine is precursor of NO, the observation indicates a role for NO in insulin secretion from beta cells. We recently reported that i.v. L-arginine elicited insulin secretion in anaesthetized rats by a mechanism that was partly NO dependent. The aim of the present study was to assess if the insulin secretory response to an intravenous infusion of glucose also requires an intact NO formation. Anaesthetized rats were given D-glucose (100 mg kg-1 min-1 i.v. for 30 min). Plasma insulin (PI), blood glucose (BG) levels and mean arterial blood pressure (MAP) were assessed from before and until 15 min after the end of the infusion. One group of rats were untreated and served as controls. The two other groups were pretreated with either of the NO synthase inhibitors NW-nitro-L-arginine methyl ester (L-NAME, 50 mg kg-1 i.v.), or NG-monomethyl-L-arginine (L-NMMA, 100 mg kg-1 i.v.). In controls infusion of glucose elevated PI by up to 25 +/- 3 U L-1, and BG by up to 27 +/- 1 mmol L-1. Pretreatment with L-NAME elevated MAP from 74 +/- 6 to 132 +/- 4 mmHg, indicating that NO synthase was inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)
Acta Physiol Scand 1995 Sep
PMID:The insulin secretory response to intravenous glucose in the rat is independent of NO formation. 855 78


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