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  • 1
    Electronic Resource
    Electronic Resource
    URINARY NO3− EXCRETION AS AN INDICATOR OF NITRIC OXIDE FORMATION IN VIVO DURING ORAL ADMINISTRATION OF l-ARGININE OR l-NAME IN RATS (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 〈list xml:id="l1" style="custom"〉1Endothelium-derived nitric oxide (NO), a major modulator of vascular tone, is synthesized from the terminal guanidino nitrogen of l-arginine. This reaction is inhibited by analogues of l-arginine, such as N-nitro-l-arginine methyl ester (l-NAME). Many of the biological effects of NO are mediated by the second messenger cGMP. NO is rapidly oxidized to NO3− which, like cGMP, is eliminated via excretion into the urine. In a placebo controlled study, we investigated whether oral bolus administration of l-arginine and l-NAME affects the urinary excretion rates of NO3− and cGMP in Munich Wistar Frömmter (MWF) rats.2Twenty MWF rats were kept in metabolic cages and received l-arginine (3 g/kg body weight), l-NAME (50mg/kg), or placebo (0.9% saline) in randomized order. Urine samples were sequentially collected for 10 h and analysed for creatinine, NO3− and cGMP.3l-Arginine induced a slight, but prolonged increase in urine flow, whereas l-NAME induced an early, transient increase in urine flow which was followed by a decrease. Creatinine clearance decreased by 65% after l-NAME, but was not affected by l-arginine or placebo.4Urinary NO3− and cGMP excretion rates transiently increased after l-arginine (NO3−: + 29%; cGMP: + 16%) for 4–5h, whereas l-NAME induced an immediate, pronounced and lasting inhibition of urinary NO3− and cGMP excretion (NO3−:-76%; cGMP:-46%). Urinary NO3− and cGMP excretions were significantly correlated (r = 0.755; P〈 0.001).5Urinary excretion rates of NO3− and cGMP, expressed as μmol/h, were correlated to urine flow (mL/h; r = 0.617 and 0.649, respectively; both P〈0.05), whereas after correction by urinary creatinine (μmol/mmol creatinine) no correlation with urine flow was observed, indicating that these excretion rates were independent of renal excretory function. Thus we conclude that changes in the urinary excretion rates of NO3− and cGMP represent changes in NO production rates in vivo when expressed in relation to urinary creatinine. Urinary NO3− and cGMP excretion is modulated by acute NO synthase inhibition or substrate provision.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb03055.x
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  • 2
    Electronic Resource
    Electronic Resource
    INFLUENCE OF PROSTAGLANDIN INHIBITION ON DIHYDRALAZINE INDUCED ACUTE EFFECTS IN PATIENTS WITH ESSENTIAL HYPERTENSION (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 12 (1985), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In order to determine whether vasodilator prostaglandins (PG) contribute to the acute vascular and endocrine responses to intravenously administered dihydralazine, we examined its effects on systolic and diastolic blood pressure (BP), heart rate (HR), plasma renin activity (PRA) and the plasma catecholamines (CA) noradrenaline (NA), adrenaline (A) and dopamine (DA) as well as on sodium, potassium and creatinine clearance (CNa, CK and CCr respectively), urinary flow rate, urinary catecholamines (NA, A, DA) and iPGE2 and i6-keto-PGF1α excretion rate in six patients (three females, three males) with essential hypertension before and after PG synthesis inhibition by the nonsteroidal, anti-inflammatory agent diclofenac.2. Diclofenac, which reduced urinary iPGE2 and i6-keto-PGF1α, excretion by 62% (P= 0.026) and 45% (P= 0.037), respectively, antagonized dihydralazine induced diastolic BP reduction (P= 0.0009), HR increase (P= 0.01), noradrenaline and adrenaline increase in plasma (P= 0.02 and P= 0.05, respectively), increase in urine flow rate (P= 0.03), sodium clearance (P= 0.01) and tended to reduce PRA.3. We conclude that dihydralazine-mediated changes can be reduced by cyclooxygenase inhibition, most likely on the basis of a reduction of its effect on peripheral resistance, thereby leading to less reflex activation of the sympathetic nervous and renin-angiotensin systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1985.tb00306.x
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  • 3
    Electronic Resource
    Electronic Resource
    Differential inhibition of human platelet aggregation and thromboxane A2 formation by L-arginine in vivo and in vitro (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1998), S. 143-150 
    Details
    ISSN: 1432-1912
    Keywords: Key words Nitric oxide ; Cyclic GMP ; Calcium ; Hirudin ; Molsidomine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We compared the effects of L-arginine (L-ARG), the precursor of endogenous NO, on platelet aggregation and thromboxane A2 formation in vivo and in vitro. Human platelet-rich plasma (PRP) was anticoagulated with citrate (which decreases extracellular Ca2+) or with recombinant hirudin (which does not affect extracellular Ca2+). Two groups of 10 healthy male volunteers received intravenous infusions of L-ARG (30 g or 6 g, 30 min) or placebo. Blood was collected immediately before and at the end of the infusions for aggregation by ADP or collagen. Infusion of L-ARG inhibited ADP-induced aggregation in PRP anticoagulated with citrate by 37.5 ± 6.3% (P 〈 0.05). In PRP anticoagulated with hirudin, aggregation was inhibited by 33.6 ± 16.0% (P 〈 0.05). L-ARG infusion also inhibited platelet TXB2 formation and slightly, but not significantly decreased the urinary excretion rate of 2,3-dinor-TXB2; cGMP concentrations in PRP were significantly elevated during L-arginine infusion. In vitro preincubation with L-ARG (10 μM–2.5 mM) inhibited platelet aggregation in PRP anticoagulated with r-hirudin, but not citrate. This effect was stereospecific for L-arginine, as D-arginine had no effect. It was dependent upon NO synthase activity, as indicated by increased cGMP levels in PRP. Moreover, both the NOS inhibitor L-NMMA and the inhibitor of soluble guanylyl cyclase ODQ antagonized the effects of L-ARG. Haemoglobin, an extracellular scavenger of NO, partly antagonized the antiplatelet effects of L-ARG. 8-Br-cyclic GMP and the exogenous NO donor linsidomine inhibited aggregation in PRP anticoagulated with citrate or r-hirudin. The inhibitory effects of L-ARG on platelet aggregation in vitro were paralleled by increased cyclic GMP levels; L-ARG also inhibited platelet TXB2 formation in PRP anticoagulated with r-hirudin, but not citrate. We conclude that the L-arginine/NO pathway is present in human platelets as a Ca2+-dependent anti-aggregatory pathway. In vivo the formation of NO from L-ARG by endothelial cells may contribute to the platelet-inhibitory effects of L-ARG. NO-releasing compounds like linsidomine inhibit platelet aggregation in vitro independent of extracellular Ca2+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005148
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  • 4
    Electronic Resource
    Electronic Resource
    Thimerosal induces endothelium-dependent vascular smooth muscle relaxations by interacting with thiol groups (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 501-507 
    Details
    ISSN: 1432-1912
    Keywords: Thimerosal ; Endothelium-dependent relaxation ; Nordihydroguaiaretic acid ; Methylene blue ; Haemoglobin ; Thiol compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The sulfhydryl reagent thimerosal, as well as acetylcholine and Ca2+-ionophore A23187, produced concentration-dependent relaxations of intact rabbit aortic strips. The ability of strips to relax in response to these agents was dependent on the presence of vascular endothelium. Purposely removing the endothelium led to a complete loss of the relaxation responses. 2. Thimerosal was at least as efficacious as A23187 in inducing endothelium-dependent relaxations, but its relaxations developed much slower than those induced by A23187 or acetylcholine. 3. A small concentration of thimerosal that had no appreciable effect by itself, potentiated the relaxing response to acetylcholine in endothelium-intact preparations. 4. Endothelium-dependent relaxations induced by larger concentrations of thimerosal, as well as relaxations produced by acetylcholine, were inhibited by the antioxidant and lipoxygenase inhibitor nordihydroguaiaretic acid, by haemoglobin, and by the inhibitor of soluble guanylate cyclase methylene blue. Indomethacin had no effect on these relaxations. 5. The thiol compounds glutathion, 2-mercaptoethanol and a low concentration of dithiothreitol prevented (and reversed) relaxations induced by thimerosal, but had little or no effect on ACh relaxations. A high concentration of dithiothreitol also markedly inhibited the ACh relaxation. 6. These results are consistent with the hypothesis that thimerosal stimulates endothelial cells to produce a relaxing substance whose properties are similar or the same as those of the endothelium-derived relaxing factor (EDRF) released in response to acetylcholine or A23187. The biochemical mechanism by which thimerosal induces the formation and/or release of this relaxing substance is likely to be different from ACh. Unlike ACh, thimerosal seems to interact with thiol groups (probably of acyltransferase enzymes) when inducing relaxation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569393
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  • 5
    Electronic Resource
    Electronic Resource
    Analysis of leukotriene B4 as free acid and its δ-lactone by high-performance liquid chromatography: a study on the stability and formation of leukotriene B4 δ-lactone (1993)
    Springer
    Fresenius' Zeitschrift für analytische Chemie 347 (1993), S. 376-381 
    Details
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Reversed-phase high-performance liquid chromatography (RP-HPLC) with UV detection (270 nm) was applied to study the stability of LTB4 δ-lactone in aqueous solutions and its chemical formation from LTB4. LTB4 δ-lactone was found to be unstable in aqueous buffered solutions (pH range 4 to 8) and was converted in a pH and time depending manner mainly to LTB4 and most probably to an isomer of LTB4 δ-lactone. This compound was spontaneously converted to LTB4 δ-lactone when incubated in the buffers and exists in equilibrium with LTB4 δ-lactone at a molar ratio of about 1:1. Incubation of LTB4 in buffers (pH 4, 6 and 8) and human plasma did not result in formation of detectable amounts of LTB4 δ-lactone. Conversion of LTB4 into its δ-lactone form in a yield of 62±6% (mean ± SD, n=3) was achieved by treatment of LTB4 with a mixture of acetic acid, acetic acid anhydride and granular calcium chloride (1/5/3, v/v/w %) in ethylacetate. Evidence for LTB4δ-lactone formation from LTB4 under these conditions was demonstrated by gas chromatography-mass spectrometry.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00323825
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  • 6
    Electronic Resource
    Electronic Resource
    Determination of nitrite as pentafluorobenzyl derivative by RP-HPLC and UV detection with and without ion-pair extraction (1992)
    Springer
    Fresenius' Zeitschrift für analytische Chemie 344 (1992), S. 256-260 
    Details
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary A reversed-phase high-performance liquid chromatographic (RP-HPLC) method with UV detection (270 nm) for the determination of nitrite as its pentafluorobenzyl derivative with and without ion-pair extraction is described. Ion-pair extraction of nitrite from aqueous solutions was performed by using a 1 mol/l solution of the liquid ion exchanger methyltrioctylammonium chloride in toluene. The residue of the ion-pair extraction or an aliquot of an aqueous nitrite solution or of a biological fluid (100 μl) were treated with 400 μl of acetone and 10 μl of pentafluorobenzyl bromide. Nitrite was converted into its pentafluorobenzyl derivative by heating at 50°C for 90 min. After evaporation of acetone the aqueous phases were diluted with 100 to 400 μl of methanol, and up to 100 μl were injected into the RP-HPLC system. The method allows accurate analysis of nitrite in the presence of nitrate directly in aqueous solutions and biological fluids in concentrations down to 2.0 mg/l. The method is also applicable to the determination of nitrate following its reduction to nitrite by cadmium.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00324985
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  • 7
    Electronic Resource
    Electronic Resource
    Analysis of nitrite and nitrate as 1-nitro-2,4,6-trimethoxybenzene derivatives by reversed-phase HPLC with UV-detection (1992)
    Springer
    Fresenius' Zeitschrift für analytische Chemie 342 (1992), S. 95-97 
    Details
    ISSN: 1618-2650
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary A reversed-phase HPLC method for the determination of nitrite and nitrate in aqueous solutions, biological buffers and human urine is described. The method is based on the conversion of nitrite and nitrate into their 1-nitro-2,4,6-trimethoxybenzene (NTBM) derivatives by using 1,3,5-trimethoxybenzene and concentrated sulphuric acid. NTMB is extracted by benzene, the solvent evaporated, the residue reconstructed in methanol/water (3/4, v/v) and subsequently analyzed by reversed-phase HPLC and UV detection (360 nm). The specificity of the nitration reaction, good reproducibility (C.V. 6.2%) and high sensitivity (8.4 ng nitrite) show the applicability of this method to the quantitative analysis of nitrite and nitrate in several matrices including human urine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00321700
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  • 8
    Electronic Resource
    Electronic Resource
    Analysis of leukotrienes, prostaglandins, thromboxane B2 and their metabolites by capillary isotachophoresis (1993)
    Weinheim : Wiley-Blackwell
    Electrophoresis 14 (1993), S. 664-666 
    Details
    ISSN: 0173-0835
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: An analytical capillary isotachophoretic method for the analysis of the eicosanoids leukotriene E4, leukotriene B4, prostaglandins E1 and E2, 6-keto-prostaglandin F1α, thromboxane B2, and their metabolites of ω- and/or β-oxidation is described. The method is based on anionic separation and detection by UV absorbance (254 nm) and conductivity and allows simultaneous analysis of the primary compounds and their corresponding major urinary metabolites. The method was applicable to the qualitative and quantitative analysis of prostaglandin E1 in a drug preparation.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/elps.11501401104
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