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  1. #1
    Registered User Disturbed0Ne's Avatar
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    Is there a thing as too much nitric-oxide?

    As the title suggests, is there such a thing as too much nitric-oxide in your system before a workout.

    I've been an avid user of GN Superpump and recently recieved a gift from a buddy, Optimum Nutrition's Nitric Boost.

    The ON product boosts "short-term" NO levels, while in my own experience, Superpump can keep me jacked up for about an hour or longer.

    Is it safe to take the two concurrently, or is there a possibility of adverse effects?

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  2. #2
    garantead KillDowzer's Avatar
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    Common rule is too much of anything is bad.


    Do you think that much nitric oxide is bad? Does it feel bad? Do you inderstand the properties of nitric oxide?
    *DISCLAIMER: Killdowzer is not responsible for advice he gives or the posts he posts.
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  3. #3
    Registered User BioStrong's Avatar
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    First of all when you take "pump" product you are not taking nitric oxide, not even close. At best you are taking precursors to nitric oxide. Your body closely regulates blood pressure and thus closely regulates nitric oxide production. You are not going to produce too much nitric oxide from supplements available now. Although there would be side effects from consuming too much of these type of products.
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  4. #4
    Title Town [Green Bay] ebongo91's Avatar
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    It may not be the nitric oxide that you OD on, but the other ingredients in the products. You are not just taking arginine, you are getting caffeine, sugar, guarana, maybe creatine, etc...
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  5. #5
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    Originally Posted by Disturbed0Ne View Post
    As the title suggests, is there such a thing as too much nitric-oxide in your system before a workout.

    I've been an avid user of GN Superpump and recently recieved a gift from a buddy, Optimum Nutrition's Nitric Boost.

    The ON product boosts "short-term" NO levels, while in my own experience, Superpump can keep me jacked up for about an hour or longer.

    Is it safe to take the two concurrently, or is there a possibility of adverse effects?

    -0Ne
    Heres a tip: ON Nitric Boost only contains Arginine. Arginine doesn't improve Nitric Oxide levels. Your buddy gave it to you because he knows it does nothing.
    Don't tell me what you want to do, do it.
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  6. #6
    Registered User Renopurtell0000's Avatar
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    Thumbs down truth about L- arginine

    Originally Posted by On Fire View Post
    Heres a tip: ON Nitric Boost only contains Arginine. Arginine doesn't improve Nitric Oxide levels. Your buddy gave it to you because he knows it does nothing.
    well i don't claim to know much myself but here is a scholarly abstract article clearly stating that the ingestion and biosynthesis of l-arginine does increase plasma and POTENT n.o. levels via NO3 arginase and urea cycle.

    soooooo.. maybe you need to do a little more research before spouting at then gums like at infant?! idk just saying. research.
    Had to copy and paste the article cause i'm a noob class, just like i said. ha.

    Articles
    L-Arginine Induces Nitric Oxide–Dependent Vasodilation in Patients With Critical Limb Ischemia
    A Randomized, Controlled Study
    Stefanie M. Bode-Böger, MD; Rainer H. Böger, MD; Heiko Alfke, MD; Doris Heinzel, MD; Dimitrios Tsikas, PhD; Andreas Creutzig, MD; Klaus Alexander, MD; Jürgen C. Frölich, MD
    + Author Affiliations

    From the Institute of Clinical Pharmacology (S.M.B.-B., R.H.B., D.H., D.T., J.C.F.) and Department of Angiology (H.A., A.C., K.A.), Medical School, Hannover, Germany.

    Abstract

    Background L-Arginine is the precursor of endogenous nitric oxide (NO), which is a potent vasodilator acting via the intracellular second-messenger cGMP. In healthy humans, L-arginine induces peripheral vasodilation and inhibits platelet aggregation due to an increased NO production. Prostaglandin E1 (PGE1) induces peripheral vasodilation via stimulating prostacyclin receptors.

    Methods and Results We investigated the effects of one intravenous infusion of L-arginine (30 g, 60 minutes) or PGE1 (40 μg, 60 minutes) versus those of placebo (150 mL 0.9% saline, 60 minutes) on blood pressure, peripheral hemodynamics, and urinary NO3− and cGMP excretion rates in patients with critical limb ischemia (peripheral arterial occlusive disease stages Fontaine III or IV). Blood flow in the femoral artery was significantly increased by L-arginine (+42.3±7.9%, P<.05) and by PGE1 (+31.0±10.2%, P<.05) but not by placebo (+4.3±13.0%, P=NS). Urinary NO3− excretion increased by 131.8±39.5% after L-arginine (P<.05) but only by 32.3±17.2% after PGE1 (P=NS). Urinary cGMP excretion increased by 198.7±84.9% after L-arginine (P<.05) and by 94.2±58.8% after PGE1 (P=NS). Both urinary index metabolites were unchanged by placebo.

    Conclusions We conclude that intravenous L-arginine induces NO-dependent peripheral vasodilation in patients with critical limb ischemia. These effects are paralleled by increased urinary NO3− and cGMP excretion, indicating an enhanced systemic NO production. Increased urinary NO3− excretion may be a sum effect of NO synthase substrate provision (L-arginine) and increased shear stress (PGE1 and L-arginine).

    The endothelium has been identified as a source of mediators that protect the vascular wall against vasospasm and thrombotic occlusion.1 These mediators include prostacyclin, a vasodilator and antiaggregatory prostaglandin,2 and nitric oxide (NO), which is synthesized from the terminal guanidino nitrogen of the amino acid precursor L-arginine.3 NO has been shown to account for the biological activity of the endothelium-derived relaxing factor in the cardiovascular system.4 These actions, mainly relaxation of vascular smooth muscle and inhibition of platelet aggregation and adhesion, are mediated by the intracellular second-messenger cGMP.5 NO is very rapidly oxidized to NO3− in vivo,6 which is subsequently excreted into the urine.7 8 As NO itself can hardly be measured in vivo, NO3− has been suggested to be a suitable index metabolite for the determination of NO formation rates in vivo.8 9 We have recently shown that intravenous L-arginine induces peripheral vasodilation, inhibits platelet aggregation, and concomitantly increases urinary NO3− and cGMP excretion rates in healthy humans.10 The release and/or biological activity of endothelium-derived relaxing factor/NO has been shown to be impaired in atherosclerotic arteries,11 12 which is in accordance with the endothelial injury hypothesis of atherosclerosis.13 Exogenous administration of L-arginine restores endothelium-dependent relaxations in experimental atherosclerosis.14 15 16 However, although L-arginine was also shown to enhance acetylcholine-induced, endothelium-dependent vasodilation in hypercholesterolemic or atherosclerotic patients,17 it has been disputed whether L-arginine is capable of inducing vasodilation in these patients.18

    The biological activity of prostacyclin is also decreased in atherosclerosis, as the homeostasis between the vasoconstrictor thromboxane A2 and prostacyclin is shifted in favor of thromboxane.19 20 Infusion of prostaglandin (PG)E1, which stimulates prostacyclin receptors and thus substitutes its deficient biological activity, has been used as pharmacotherapy for peripheral arterial occlusive disease in Germany and several other countries.21 22

    In the present study, we investigated whether L-arginine, given as a single intravenous infusion, induces vasodilation in the more severely affected lower limb of patients with critical limb ischemia and whether the possible hemodynamic effects are related to an increased NO production (using the urinary excretion rates of NO3− and cGMP as index parameters for systemic NO formation in vivo). We compared the effects of L-arginine with those of PGE1 as an NO/cGMP-independent vasodilator and with those of placebo.

    Patients and Study Design
    Ten male patients with critical limb ischemia (peripheral arterial occlusive disease stages Fontaine III or IV) received a single intravenous infusion of L-arginine (Fresenius AG; 30 g dissolved in 150 mL 0.9% saline, pH 6.5) or PGE1 (Prostavasin, Schwarz Pharma; 40 μg dissolved in 150 mL 0.9% saline) into an antecubital vein over 60 minutes. Both substances were administered in randomized order with a washout period of at least 2 days between them. Another group of six patients with critical limb ischemia received a single intravenous infusion of placebo (150 mL 0.9% saline, 60 minutes). All patients had angiographically proven femoropopliteal occlusions and additional distal stenoses of the crural arteries. None had proximal hemodynamically relevant stenoses of the iliac vessels. The cardiovascular risk factors and parallel diseases of the two groups of patients are given in Table 1⇓, and the mean plasma cholesterol and triglyceride levels are given in Table 2⇓. Each patient gave written informed consent to participation in the study, which had been approved by the Hannover Medical School Ethics Committee. Comedication, which was kept constant throughout the study period, is given in Table 3⇓. At the beginning of each study day, each patient emptied his bladder. A mild oral volume loading (using demineralized water) was started with 3 mL/kg body wt initially and continued during the study period with 1 to 2 mL·kg−1·h−1 adjusted to the individual hourly urine volumes. Each participant remained in the supine position for 60 minutes before and 30 minutes after the infusion.

    View this table:
    In this window In a new window
    Table 1.
    Characteristics of Patients Participating in the Study, Including Fontaine Stage Classification of Peripheral Arterial Disease and Risk Profile/Parallel Diseases

    Table 2.
    Plasma Cholesterol and Triglyceride Levels

    Comedications of Study Patients

    During 1 hour before and 3 hours after the beginning of the infusion, urine was collected in hourly intervals and immediately frozen for the determination of urinary NO3− and cGMP concentrations. At baseline and at the end of the infusions, a venous blood sample was drawn with EDTA for the determination of plasma arginine levels.

    At 60 minutes before, during, and for 20 minutes after the end of the infusion, blood pressure and heart rate were recorded every 5 minutes by the standard sphygomanometric method with an automatic device (Boso digital II, Bosch & Sohn).

    Duplex Measurements of Femoral Arterial Blood Flow
    Blood flow velocity was measured by image-directed duplex ultrasonography before the infusion and at its end in a segment of the common femoral artery with a circular cross section. Measurements were made with a DRF 400 image-directed duplex ultrasound system (Diasonics-Sonotron) with a transducer combining 7.5-MHz B-mode imaging and 3-MHz pulsed Doppler beams. Blood flow volume was automatically calculated as the product of the cross-sectional area and the time-averaged blood velocity from seven repeated measurements.23 The investigator performing the duplex measurements was blinded to the treatment.

    Biochemical Assays
    Urinary NO2−/NO3− was determined as its pentafluorobenzyl derivative by gas chromatography–mass spectrometry (GC-MS) as described previously.24 25 Briefly, 100-μL aliquots of urine were spiked with 250 ng of [15N]NO3− (MSD Isotopes Merck Frosst) as internal standard, acidified with 20 μL of 0.1 N HCl, and treated with 5 mg cadmium for 10 minutes at room temperature. The suspension was then centrifuged; the supernatant decanted and alkalinized with 10 μL of 4 N NaOH, treated with 500 μL of cold acetone (−20°C), and centrifuged. Then, 5 μL of pentafluorobenzyl bromide was added to the decanted supernatant, and the mixture was allowed to react for 75 minutes at 50°C. After being cooled to room temperature, acetone was removed under nitrogen, and the residue was extracted with 1 mL of toluene. The toluene phase was taken up and dried over Na2SO4. Then 1-μL aliquots were injected into the GC-MS device.

    GC-MS was carried out on a triple-stage quadrupole mass spectrometer TSQ 45 interfaced with a gas chromatograph 9611 (Finnigan MAT). An OV-1 fused silica capillary column (25×0.25 mm ID, 0.25-μm film thickness) from Machery-Nagel was used with helium as the carrier gas (55 kPa). Negative ions were produced by chemical ionization using methane as the reactant gas (65 Pa) at an electron energy of 90 eV and an electron current of 0.2 mA. Quantification was performed by selected ion monitoring at m/z 46 for endogenous NO2−/NO3− and m/z 47 for the internal standard. The detection limit of the method was 20 fmol nitrite or nitrate. Intra-assay variability was less than 3.8%.

    For the determination of cGMP levels, urine samples were thawed and centrifuged at 2500g (4°C; 10 minutes). Supernatants were diluted 1:500 in phosphate buffered saline and acetylated by a mixture of acetic acid anhydride/triethylamine. cGMP content was measured by radioimmunoassay using [125I]cGMP as a tracer and globulin precipitation. The detection limit of the assay was 160 fmol/mL.

    Urinary creatinine was determined spectrophotometrically with the alkaline picric acid method in an automatic analyzer (Beckman). The urinary excretion rates of NO3− and cGMP were corrected by urinary creatinine concentration.

    Plasma arginine levels were determined spectrophotometrically after conversion to urea according to the method of Bacchus and London.26

    Femoral arterial blood flow was enhanced by 42.3±7.9% during L-arginine infusion (P<.05) and by 31.0±10.2% during PGE1 infusion (P<.05) but remained unchanged during placebo infusion (+4.3±13.0%, P=NS) (Fig 1⇓). There was no significant difference between both active treatments. However, blood flow further increased until 30 minutes after the end of L-arginine infusion, whereas after the end of PGE1 infusion blood flow immediately began to decrease. This effect was due to an increased blood flow velocity (+56% after L-arginine, +29% after PGE1), whereas the femoral artery diameter remained unchanged (Table 4⇓). Furthermore, L-arginine had a more pronounced effect on systolic and diastolic blood pressures than PGE1, as assessed by comparison of the area under the blood pressure–time curves (P<.05), and placebo had no affect on blood pressure (Fig 2⇓). Neither of the infusions significantly affected heart rates.
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  7. #7
    I'll Mod Til I'm Dead ironwill2008's Avatar
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    Originally Posted by Renopurtell0000 View Post
    well i don't claim to know much myself but here is a scholarly abstract article clearly stating that the ingestion and biosynthesis of l-arginine does increase plasma and POTENT n.o. levels via NO3 arginase and urea cycle.

    soooooo.. maybe you need to do a little more research before spouting at then gums like at infant?! idk just saying. research..................




    Methods and Results We investigated the effects of one intravenous infusion
    As per the bolded,, the study you cited is irrelevant to supplement forms of arginine, the topic of the OP, which are taken orally.


    It's always a good idea to read the entire text rather than just the study title before posting.
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  8. #8
    Omega Weapon EjnarKolinkar's Avatar
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    http://examine.com/supplements/Arginine/

    Examine is a decent resource. One ingredient linked. Common problem is gastro upset or diarrhea with too much arginine.

    Superpump has a variety of ingredients, you can look each up and see what you would want to be cautious of and or if you feel the supplement(s) has the potential to be beneficial to you. Research what you take before you take it, don't rely on others to do so for you. Unless you are looking at something like this

    http://www.jissn.com/content/11/1/20
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  9. #9
    retired lifter rhadam's Avatar
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    Originally Posted by Renopurtell0000 View Post
    well i don't claim to know much myself but here is a scholarly abstract article clearly stating that the ingestion and biosynthesis of l-arginine does increase plasma and POTENT n.o. levels via NO3 arginase and urea cycle.

    soooooo.. maybe you need to do a little more research before spouting at then gums like at infant?! idk just saying. research.
    Had to copy and paste the article cause i'm a noob class, just like i said. ha.

    Articles
    L-Arginine Induces Nitric Oxide–Dependent Vasodilation in Patients With Critical Limb Ischemia
    A Randomized, Controlled Study
    Stefanie M. Bode-Böger, MD; Rainer H. Böger, MD; Heiko Alfke, MD; Doris Heinzel, MD; Dimitrios Tsikas, PhD; Andreas Creutzig, MD; Klaus Alexander, MD; Jürgen C. Frölich, MD
    + Author Affiliations

    From the Institute of Clinical Pharmacology (S.M.B.-B., R.H.B., D.H., D.T., J.C.F.) and Department of Angiology (H.A., A.C., K.A.), Medical School, Hannover, Germany.

    Abstract

    Background L-Arginine is the precursor of endogenous nitric oxide (NO), which is a potent vasodilator acting via the intracellular second-messenger cGMP. In healthy humans, L-arginine induces peripheral vasodilation and inhibits platelet aggregation due to an increased NO production. Prostaglandin E1 (PGE1) induces peripheral vasodilation via stimulating prostacyclin receptors.

    Methods and Results We investigated the effects of one intravenous infusion of L-arginine (30 g, 60 minutes) or PGE1 (40 μg, 60 minutes) versus those of placebo (150 mL 0.9% saline, 60 minutes) on blood pressure, peripheral hemodynamics, and urinary NO3− and cGMP excretion rates in patients with critical limb ischemia (peripheral arterial occlusive disease stages Fontaine III or IV). Blood flow in the femoral artery was significantly increased by L-arginine (+42.3±7.9%, P<.05) and by PGE1 (+31.0±10.2%, P<.05) but not by placebo (+4.3±13.0%, P=NS). Urinary NO3− excretion increased by 131.8±39.5% after L-arginine (P<.05) but only by 32.3±17.2% after PGE1 (P=NS). Urinary cGMP excretion increased by 198.7±84.9% after L-arginine (P<.05) and by 94.2±58.8% after PGE1 (P=NS). Both urinary index metabolites were unchanged by placebo.

    Conclusions We conclude that intravenous L-arginine induces NO-dependent peripheral vasodilation in patients with critical limb ischemia. These effects are paralleled by increased urinary NO3− and cGMP excretion, indicating an enhanced systemic NO production. Increased urinary NO3− excretion may be a sum effect of NO synthase substrate provision (L-arginine) and increased shear stress (PGE1 and L-arginine).

    The endothelium has been identified as a source of mediators that protect the vascular wall against vasospasm and thrombotic occlusion.1 These mediators include prostacyclin, a vasodilator and antiaggregatory prostaglandin,2 and nitric oxide (NO), which is synthesized from the terminal guanidino nitrogen of the amino acid precursor L-arginine.3 NO has been shown to account for the biological activity of the endothelium-derived relaxing factor in the cardiovascular system.4 These actions, mainly relaxation of vascular smooth muscle and inhibition of platelet aggregation and adhesion, are mediated by the intracellular second-messenger cGMP.5 NO is very rapidly oxidized to NO3− in vivo,6 which is subsequently excreted into the urine.7 8 As NO itself can hardly be measured in vivo, NO3− has been suggested to be a suitable index metabolite for the determination of NO formation rates in vivo.8 9 We have recently shown that intravenous L-arginine induces peripheral vasodilation, inhibits platelet aggregation, and concomitantly increases urinary NO3− and cGMP excretion rates in healthy humans.10 The release and/or biological activity of endothelium-derived relaxing factor/NO has been shown to be impaired in atherosclerotic arteries,11 12 which is in accordance with the endothelial injury hypothesis of atherosclerosis.13 Exogenous administration of L-arginine restores endothelium-dependent relaxations in experimental atherosclerosis.14 15 16 However, although L-arginine was also shown to enhance acetylcholine-induced, endothelium-dependent vasodilation in hypercholesterolemic or atherosclerotic patients,17 it has been disputed whether L-arginine is capable of inducing vasodilation in these patients.18

    The biological activity of prostacyclin is also decreased in atherosclerosis, as the homeostasis between the vasoconstrictor thromboxane A2 and prostacyclin is shifted in favor of thromboxane.19 20 Infusion of prostaglandin (PG)E1, which stimulates prostacyclin receptors and thus substitutes its deficient biological activity, has been used as pharmacotherapy for peripheral arterial occlusive disease in Germany and several other countries.21 22

    In the present study, we investigated whether L-arginine, given as a single intravenous infusion, induces vasodilation in the more severely affected lower limb of patients with critical limb ischemia and whether the possible hemodynamic effects are related to an increased NO production (using the urinary excretion rates of NO3− and cGMP as index parameters for systemic NO formation in vivo). We compared the effects of L-arginine with those of PGE1 as an NO/cGMP-independent vasodilator and with those of placebo.

    Patients and Study Design
    Ten male patients with critical limb ischemia (peripheral arterial occlusive disease stages Fontaine III or IV) received a single intravenous infusion of L-arginine (Fresenius AG; 30 g dissolved in 150 mL 0.9% saline, pH 6.5) or PGE1 (Prostavasin, Schwarz Pharma; 40 μg dissolved in 150 mL 0.9% saline) into an antecubital vein over 60 minutes. Both substances were administered in randomized order with a washout period of at least 2 days between them. Another group of six patients with critical limb ischemia received a single intravenous infusion of placebo (150 mL 0.9% saline, 60 minutes). All patients had angiographically proven femoropopliteal occlusions and additional distal stenoses of the crural arteries. None had proximal hemodynamically relevant stenoses of the iliac vessels. The cardiovascular risk factors and parallel diseases of the two groups of patients are given in Table 1⇓, and the mean plasma cholesterol and triglyceride levels are given in Table 2⇓. Each patient gave written informed consent to participation in the study, which had been approved by the Hannover Medical School Ethics Committee. Comedication, which was kept constant throughout the study period, is given in Table 3⇓. At the beginning of each study day, each patient emptied his bladder. A mild oral volume loading (using demineralized water) was started with 3 mL/kg body wt initially and continued during the study period with 1 to 2 mL·kg−1·h−1 adjusted to the individual hourly urine volumes. Each participant remained in the supine position for 60 minutes before and 30 minutes after the infusion.

    View this table:
    In this window In a new window
    Table 1.
    Characteristics of Patients Participating in the Study, Including Fontaine Stage Classification of Peripheral Arterial Disease and Risk Profile/Parallel Diseases

    Table 2.
    Plasma Cholesterol and Triglyceride Levels

    Comedications of Study Patients

    During 1 hour before and 3 hours after the beginning of the infusion, urine was collected in hourly intervals and immediately frozen for the determination of urinary NO3− and cGMP concentrations. At baseline and at the end of the infusions, a venous blood sample was drawn with EDTA for the determination of plasma arginine levels.

    At 60 minutes before, during, and for 20 minutes after the end of the infusion, blood pressure and heart rate were recorded every 5 minutes by the standard sphygomanometric method with an automatic device (Boso digital II, Bosch & Sohn).

    Duplex Measurements of Femoral Arterial Blood Flow
    Blood flow velocity was measured by image-directed duplex ultrasonography before the infusion and at its end in a segment of the common femoral artery with a circular cross section. Measurements were made with a DRF 400 image-directed duplex ultrasound system (Diasonics-Sonotron) with a transducer combining 7.5-MHz B-mode imaging and 3-MHz pulsed Doppler beams. Blood flow volume was automatically calculated as the product of the cross-sectional area and the time-averaged blood velocity from seven repeated measurements.23 The investigator performing the duplex measurements was blinded to the treatment.

    Biochemical Assays
    Urinary NO2−/NO3− was determined as its pentafluorobenzyl derivative by gas chromatography–mass spectrometry (GC-MS) as described previously.24 25 Briefly, 100-μL aliquots of urine were spiked with 250 ng of [15N]NO3− (MSD Isotopes Merck Frosst) as internal standard, acidified with 20 μL of 0.1 N HCl, and treated with 5 mg cadmium for 10 minutes at room temperature. The suspension was then centrifuged; the supernatant decanted and alkalinized with 10 μL of 4 N NaOH, treated with 500 μL of cold acetone (−20°C), and centrifuged. Then, 5 μL of pentafluorobenzyl bromide was added to the decanted supernatant, and the mixture was allowed to react for 75 minutes at 50°C. After being cooled to room temperature, acetone was removed under nitrogen, and the residue was extracted with 1 mL of toluene. The toluene phase was taken up and dried over Na2SO4. Then 1-μL aliquots were injected into the GC-MS device.

    GC-MS was carried out on a triple-stage quadrupole mass spectrometer TSQ 45 interfaced with a gas chromatograph 9611 (Finnigan MAT). An OV-1 fused silica capillary column (25×0.25 mm ID, 0.25-μm film thickness) from Machery-Nagel was used with helium as the carrier gas (55 kPa). Negative ions were produced by chemical ionization using methane as the reactant gas (65 Pa) at an electron energy of 90 eV and an electron current of 0.2 mA. Quantification was performed by selected ion monitoring at m/z 46 for endogenous NO2−/NO3− and m/z 47 for the internal standard. The detection limit of the method was 20 fmol nitrite or nitrate. Intra-assay variability was less than 3.8%.

    For the determination of cGMP levels, urine samples were thawed and centrifuged at 2500g (4°C; 10 minutes). Supernatants were diluted 1:500 in phosphate buffered saline and acetylated by a mixture of acetic acid anhydride/triethylamine. cGMP content was measured by radioimmunoassay using [125I]cGMP as a tracer and globulin precipitation. The detection limit of the assay was 160 fmol/mL.

    Urinary creatinine was determined spectrophotometrically with the alkaline picric acid method in an automatic analyzer (Beckman). The urinary excretion rates of NO3− and cGMP were corrected by urinary creatinine concentration.

    Plasma arginine levels were determined spectrophotometrically after conversion to urea according to the method of Bacchus and London.26

    Femoral arterial blood flow was enhanced by 42.3±7.9% during L-arginine infusion (P<.05) and by 31.0±10.2% during PGE1 infusion (P<.05) but remained unchanged during placebo infusion (+4.3±13.0%, P=NS) (Fig 1⇓). There was no significant difference between both active treatments. However, blood flow further increased until 30 minutes after the end of L-arginine infusion, whereas after the end of PGE1 infusion blood flow immediately began to decrease. This effect was due to an increased blood flow velocity (+56% after L-arginine, +29% after PGE1), whereas the femoral artery diameter remained unchanged (Table 4⇓). Furthermore, L-arginine had a more pronounced effect on systolic and diastolic blood pressures than PGE1, as assessed by comparison of the area under the blood pressure–time curves (P<.05), and placebo had no affect on blood pressure (Fig 2⇓). Neither of the infusions significantly affected heart rates.
    LMAO did you seriously just post this chitty intravenous study? Arginine has been debunked for years. 1995 called, it wants it's broscience back.
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