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  • 1
    Electronic Resource
    Electronic Resource
    Glucosaminylmuramyl dipeptide (GMDP) modulates endothelial cell activities in vitro but has no effect on angiogenesis in vivo (1997)
    Springer
    Inflammation research 46 (1997), S. 348-353 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Glucosaminylmuramyl dipeptide — Human umbilical vein endothelial cells — ICAM-1 — CD31 — Cell adhesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective and Design: The aim of the study was to evaluate the effects of GMDP on angiogenesis in vivo and as a modulator of human umbilical vein endothelial cell proliferation, cell surface antigen expression and cell adhesion in vitro.¶Materials: Human umbilical vein endothelial cells (HUVEC), fertilized white leghorn chicken eggs, antibodies against adhesion molecules and glucosaminylmuramyl dipeptide (GMDP).¶Treatment: GMDP [0.01–100 μg/ml] applied to cell cultures for 6–72 h and to the chick chorioallantoic membrane (CAM) for four days.¶Methods: Angiogenic activity of GMDP in vivo was assessed using the CAM assay; HUVEC proliferation was measured by tritiated thymidine incorporation and cell cycle studies; cell surface antigen expression by indirect immunofluorescence and flow cytometry; cell adhesion by quantification of [3H]-thymidine labeled leukocyte adherence to HUVEC monolayers. Statistical analysis was performed using one-way ANOVA and if necessary was followed by Duncan's multiple range test for variables.¶Results: GMDP induced [3H]-thymidine incorporation in a concentration- and time-dependent manner (p 〈 0.003) and significantly increased the proportion of cells in the S phase of the cell cycle (p 〈 0.03). It weakly augmented the expression of ICAM-1 and CD31 but not adhesion of leukocytes to HUVEC monolayers GMDP was not angiogenic in the CAM assay.¶Conclusions: GMDP can modulate endothelial cell activity without the induction of angiogenesis in vivo which may have implications for its use as a therapeutic agent.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050200
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  • 2
    Electronic Resource
    Electronic Resource
    THE INHIBITION OF NITRIC OXIDE-MEDIATED RELAXATIONS IN RAT AORTA AND ANOCOCCYGEUS MUSCLE BY DIPHENYLENE IODONIUM (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of diphenylene iodonium (DPI), an inhibitor of reduced nicotinamide adenine dinucleotide phosphate-dependent oxidases (which generate superoxide anions), were studied on nitric oxide (NO)-mediated responses in isolated preparations of the rat aorta and anococcygeus muscle.2. In aortic rings, the endothelium-dependent relaxant action of acetylcholine was reduced by DPI (0.3–10 μmol/L) in a concentration-dependent manner and abolished by the NO synthase (NOS) inhibitor L-nitro-NG-arginine methylester (l-NAME; 100 μmol/L). Relaxations induced by sodium nitroprusside (SNP) or NO were not affected by DPI or l-NAME.3. In anococcygeus muscles, DPI (0.3–10 μmol/ L) as well as l-NAME (5–100 μmol/L) produced concentration-dependent reductions of relaxations produced by nitrergic nerve stimulation. Relaxations induced by NO and SNP were not affected by either DPI or l-NAME. l-Arginine (1 mmol/L) prevented the reduction of nitrergic relaxations by l-NAME but not by DPI.4. Contractions of anococcygeus muscles elicited by exogenous noradrenaline (1 μmol/ L) were not affected or were inhibited by DPI (0.3–10 μmol/L), but the contractions elicited by noradrenergic nerve stimulation were significantly enhanced by DPI and l-NAME. When noradrenergic contractions had already been maximally enhanced by l-NAME (100 μmol/L), DPI produced no further enhancement. l-Arginine (1 mmol/L) prevented the enhancement of noradrenergic contractions by l-NAME but not by DPI.5. The efflux of radioactivity induced by field stimulation from anococcygeus muscles previously incubated with [3H]-noradrenaline was not affected by either DPI or l-NAME.6. Superoxide dismutase (SOD, 100 U/mL) had no significant effects on noradrenergic contractions, nitrergic relaxations, relaxations induced by NO or the actions of DPI in the rat anococcygeus muscle.7. The results suggest that the effects of DPI in reducing the NO-mediated relaxations produced by acetylcholine in rat aortic rings and stimulation of nitrergic nerves in the rat anococcygeus muscle are due to the inhibition of NOS in these tissues. The effects of DPI were not sensitive to l-arginine, and thus the mechanism of inhibition of NOS differs from that of l-NAME.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01661.x
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  • 3
    Electronic Resource
    Electronic Resource
    EFFECTS OF HYDROXOCOBALAMIN AND HAEMOGLOBIN ON NO-MEDIATED RELAXATIONS IN THE RAT ANOCOCCYGEUS MUSCLE (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of hydroxocobalamin (Vitamin B12a) on relaxations produced by nitric oxide (NO), some NO-donating compounds and nitrergic nerve stimulation in isolated preparations of the rat anococcygeus muscle were compared with the effects of haemoglobin.2. Hydroxocobalamin (30 μmol/L) significantly reduced relaxations induced by NO (0.1–3 μmol/L) and sodium nitroprusside (SNP; 0.01–0.3 μmol/L) but did not affect relaxations induced by glyceryl trinitrate (GTN; 0.01–1 μmol/L), S-nitrosocysteine (0.1–0.3 μmol/L) or stimulation of nitrergic nerves. A higher concentration of hydroxocobalamin (100 μmol/L) slightly reduced nitrergic nerve stimulation-induced relaxations.3. Haemoglobin (10 μmol/L) blocked relaxation induced by NO and reduced relaxations induced by SNP, GTN, S-nitrosocysteine and nitrergic nerve stimulation.4. When nitrergic nerve stimulation-induced relaxations had been partially reduced by the NO synthase inhibitor l-NAME (5–10 μmol/L), hydroxocobalamin had only a weak and transient inhibitory effect.5. Noradrenergic contractions induced by field stimulation were not affected by hydroxocobalamin (30 μmol/L), but were enhanced by haemoglobin (10 μmol/L).6. The results suggest that the transmitter released from nitrergic nerves in anococcygeus muscles resembles NO-releasing compounds such as S-nitrosocysteine and GTN but not SNP or free NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01645.x
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  • 4
    Electronic Resource
    Electronic Resource
    RILMENIDINE ACTS AS A PARTIAL AGONIST AT PREJUNCTIONAL α2-ADRENOCEPTORS IN GUINEA-PIG ATRIA (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 15 (1988), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The present study was carried out to determine whether rilmenidine, a recently introduced antihypertensive agent which acts on α2-adrenoceptors, has partial agonist activity on prejunctional α2-adrenoceptors in guinea-pig atria.2. Isolated preparations of guinea-pig atria were incubated with [3H]-noradrenaline and the efflux of radioactivity induced by stimulation of intramural sympathetic nerves was used as an index of release of transmitter noradrenaline.3. Rilmenidine (1 μmol/1) inhibited noradrenaline release evoked by short trains (five, 20 and 50 pulses) of sympathetic nerve stimulation and this inhibitory effect of rilmenidine was antagonized by the α2-adrenoceptor antagonists, idazoxan (0.1 and 0.3 umol/1) and rauwolscine (0.3 umol/1) whereas it was not affected by the α1-adrenoceptor antagonist prazosin (0.1 μmol/1).4. On the other hand, rilmenidine (1 μmol/1) enhanced noradrenaline release evoked by long trains (150 and 300 pulses) of stimulation and this effect was also abolished by idazoxan (0.1 μmol/1).5. These findings suggest that the effects of rilmenidine on transmitter release depend on the degree of auto-inhibition: when the concentration of noradrenaline in the biophase of the prejunctional α2-adrenoceptors is low, rilmenidine acts as an agonist, but when the concentration is high it acts as an antagonist. Thus, rilmenidine, like clonidine, is a partial agonist on prejunctional α2-adrenoceptors in guinea-pig atria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1988.tb01016.x
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  • 5
    Electronic Resource
    Electronic Resource
    ACTIVATION OF NORADRENERGIC AND NITRERGIC MECHANISMS IN THE RAT ANOCOCCYGEUS MUSCLE BY NICOTINE (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: b1. Nicotine (10 μmol/L) produced rapidly developing but transient contractions of anococcygeus muscle isolated from rats. The magnitude of the response varied considerably between preparations. Tachyphylaxis occurred, such that no response was elicited by the same or a larger concentration in the continued presence of 10 μmol/L nicotine.2. Contractions produced by nicotine were not affected by atropine, but were abolished by Hexamethonium and the α-adrenoceptor antagonists prazosin and phentolamine. Contractions were absent in the anococcygeus muscles of rats pretreated with reserpine.3. The (α-adrenoceptor agonist UK 14304, or guanethidine, raised the tone of the anococcygeus muscle, and converted responses to field stimulation and nicotine to relaxations. Nicotine-induced relaxations were more pronounced in the presence of UK14304 than guanethidine.4. Relaxations produced by nicotine (1–18 μmol/L) were transient, and tachyphylaxis occurred. When precautions were taken to avoid tachyphylaxis, concentration-response curves could be constructed. The relaxations elicited by nicotine were abolished or greatly reduced by hexamethonium, tetrodotoxin or ω-conotoxin GVIA.5. The nitric oxide synthase inhibitor l-NG-nitroarginine methyl ester (90 μmol/L) enhanced contractile responses to field stimulation and nicotine, and markedly reduced relaxations elicited by field stimulation and nicotine in the presence of UK14304. These relaxations were restored by l-arginine (270 μmol/L).6. The results suggest that nicotine acts on nicotinic receptors of noradrenergic and nitrergic nerve terminals in the rat anococcygeus muscle, resulting in the release of noradrenaline and nitric oxide respectively.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00428.x
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  • 6
    Electronic Resource
    Electronic Resource
    INHIBITION BY ETHACRYNIC ACID OF NO-MEDIATED RELAXATIONS OF THE RAT ANOCOCCYGEUS MUSCLE (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of ethacrynic acid were studied on relaxations elicited by nitric oxide (NO), the NO-donors sodium nitroprusside (SNP) and glyceryl trinitrate (GTN), nitrergic nerve stimulation and the NO-independent agent papaverine in isolated preparations of rat anococcygeus muscles.2. Ethacrynic acid (100 μmol/L) produced complete relaxation of partially contracted anococcygeus muscles, but the tone recovered after the ethacrynic acid was washed out. Following exposure to ethacrynic acid, the relaxant responses to NO, SNP, GTN and nitrergic nerve stimulation were abolished or markedly reduced; however, the response to papaverine was only slightly reduced.3. The presence of 3 mmol/L l-cysteine during the period of exposure to ethacrynic acid prevented the inhibition of the relaxing effects of SNP, GTN and nitrergic nerve stimulation almost completely, but did not affect the slight reduction in responses to papaverine.4. The addition of l-cysteine (3 mmol/L) after incubation with ethacrynic acid did not significantly affect the inhibited responses to SNP and GTN; however, the inhibited responses to nitrergic nerve stimulation were slightly but significantly increased.5. The results suggest that endogenous sulphydryl groups are required for the actions of NO, NO-donating drugs and the nitrergic transmitter in the rat anococcygeus muscle and possibly for the synthesis or release of the nitrergic transmitter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02515.x
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  • 7
    Electronic Resource
    Electronic Resource
    EVIDENCE FOR A ROLE OF NITRIC OXIDE IN THE NEUROTRANSMITTER SYSTEM MEDIATING RELAXATION OF THE RAT ANOCOCCYGEUS MUSCLEC (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The nitric oxide (NO) synthesis inhibitor NG-monomethyl-l-arginine (l-NMMA), but not d-NMMA, inhibited the NANC-mediated relaxations of the rat anococcygeus muscle, but did not affect the relaxation produced by sodium nitroprusside.2. The inhibitory effect of l-NMMA was reversed by l-arginine but not by d-arginine, and prior exposure to l-arginine blocked the effect of l-NMMA.3. The noradrenergically mediated contractions of the anococcygeus elicited by field stimulation were slightly enhanced by l-NMMA, but the response to noradrenaline was not affected.4. The results suggest that NANC transmission in the rat anococcygeus muscle involves the generation of NO from arginine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb02404.x
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  • 8
    Electronic Resource
    Electronic Resource
    PHARMACOLOGICAL ACTIONS OF THE COENZYMES NAD(H) AND NADP(H) ON THE RAT ANOCOCCYGEUS MUSCLE (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The pharmacological actions of the oxidized and reduced forms of nicotinamide-adenosine dinucleotide (NAD, NADH) and nicotinamide-adenosine dinucleotide phosphate (NADP, NADPH) were studied on rat isolated anococcygeus muscles.2. The actions of the two nucleotides were different, but there were no apparent qualitative differences between the oxidized and reduced forms of each.3. In fully relaxed anococcygeus muscles, NADP(H) produced transient contractions that were subject to desensitization, but NAD(H) had no effect.4. NADP(H) slightly enhanced contractions elicited by noradrenergic nerve stimulation. In contrast, noradrenergic contractions were inhibited by NAD(H). NADH reduced the stimulation-induced release of noradrenaline, but enhanced contractions elicited by exogenous noradrenaline.5. In anococcygeus muscles partly contracted with guanethidine, NAD(H) produced a further sustained increase in tone; in contrast, NADP(H) mainly produced transient relaxations to which there was immediate desensitization.6. Relaxations of anococcygeus muscle elicited by nitrergic nerve stimulation were not affected by NAD. In contrast, NADP(H) reduced them.7. The actions of NAD(H) were generally the same as those of adenosine and can be attributed to activation of P1-purinoceptors since they were blocked by the selective antagonist 8-sulphophenyl-theophylline.8. The actions of NADP resembled those of the P2-purinoceptor agonist ATP to some extent, but there were some differences. As suggested by others, NADP may act on a unique receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02431.x
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  • 9
    Electronic Resource
    Electronic Resource
    EFFECTS OF ARGININOSUCCINIC ACID ON NITRIC OXIDE-MEDIATED RELAXATIONS IN RAT AORTA AND ANOCOCCYGEUS MUSCLE (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Argininosuccinic acid (ASA), a naturally occurring NG derivative of arginine, and the nitric oxide synthase (NOS) inhibitor JVG-nitro-L-arginine methyl ester (l-NAME) were compared for their ability to reduce responses to nitric oxide (NO) derived from endothelial cells (aorta) and nitrergic nerves (anococcygeus muscle).2. In isolated rings of rat aorta, endothelium-dependent relaxation responses to acetylcholine were abolished by l-NAME (0.1 mmol/L) and were reduced by ASA (0.1 and 0.3 mmol/L). Relaxations induced by sodium nitroprusside (SNP) were not affected by l-NAME but were reduced by ASA.3. In rat isolated anococcygeus muscles, relaxations elicited by nitrergic nerve stimulation at 1 Hz were abolished by l-NAME (0.1 mmol/L) but were only slightly reduced by ASA (1 mmol/L). The effect of ASA was not sustained. l-Arginine (1 mmol/L) prevented the effect of L-NAME but not that of ASA. Neither ASA or l-NAME inhibited SNP-induced relaxation in the anococcygeus muscle.4. The results suggest that ASA inhibits NOS but this does not totally account for its effects in reducing NO-mediated relaxations produced by the endothelium-dependent vasodilator acetylcholine in rat aortic rings and stimulation of nitrergic nerves in the rat anococcygeus muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1992.tb00465.x
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  • 10
    Electronic Resource
    Electronic Resource
    MEDIATORS OF NICOTINE-INDUCED RELAXATIONS OF THE RAT GASTRIC FUNDUS (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Relaxations of strips of rat gastric fundus were elicited with nicotine (100 μmol/L), nitric oxide (NO; 30 μmol/L), sodium nitroprusside (SNP; 100 nmol/L) and vasoactive intestinal polypeptide (VIP; 1 nmol/L).2. Methylene blue (30 μmol/L), an inhibitor of soluble guanylate cyclase, reduced relaxations elicited by NO and nicotine, but not those elicited by VIP.3. Chymotrypsin (1 U/mL) abolished VIP-induced relaxations and reduced nicotine-induced relaxations, but had no effect on SNP-induced relaxations.4. NG-nitro-l-arginine methyl ester (l-NAME; 100 μmol/L), an inhibitor of NO synthase, reduced relaxations elicited by nicotine, but not those elicited by SNP or VIP.5. When nicotine-induced relaxations had been reduced by either l-NAME or chymotrypsin, the addition of the other agent produced a greater reduction. However, the relaxations were not abolished.6. Nicotine-induced relaxations were abolished by tetrodotoxin (1 μmol/L) or hexamethonium (100 μmol/L), indicating that they were due to activation of neuronal nicotinic receptors. Their reduction by methylene blue and l-NAME indicates that an NO-like mediator was involved. Their reduction by chymotrypsin indicates that a VIP-like peptide was involved. However, since they were not abolished by a combination of l-NAME and chymotrypsin, it appears that at least one more as yet unidentified mediator may be involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01723.x
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