scholarly journals Steady-state nitric oxide concentrations during denitrification.

1990 ◽  
Vol 265 (20) ◽  
pp. 11535-11538 ◽  
Author(s):  
J Goretski ◽  
O C Zafiriou ◽  
T C Hollocher
Keyword(s):  
Nitric Oxide ◽  
Steady State

scholarly journals Contribution of adenosine to compensatory dilation in hypoperfused contracting human muscles is independent of nitric oxide

2011 ◽  
Vol 110 (5) ◽  
pp. 1181-1189 ◽  
Author(s):  
Darren P. Casey ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Steady State ◽  
Arterial Pressure ◽  
Brachial Artery ◽  
Adenosine Receptor ◽  
Receptor Blockade ◽  
Independent Manner ◽  
Control Value ◽  
Percent Recovery

We previously demonstrated that nitric oxide (NO) contributes to compensatory vasodilation in the contracting human forearm subjected to acute hypoperfusion. We examined the potential role of an adenosine-NO interaction to this response in 17 male subjects (25 ± 2 yr). In separate protocols subjects performed rhythmic forearm exercise (20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included exercise before inflation, exercise with inflation, and exercise after deflation (3 min each). Forearm blood flow (FBF; ultrasound) and local [brachial artery catheter pressure (BAP)] and systemic [mean arterial pressure (MAP); Finometer] arterial pressure were measured. In protocol 1 ( n = 10), exercise was repeated during nitric oxide synthase inhibition [ NG-monomethyl-l-arginine (l-NMMA)] alone and during l-NMMA-aminophylline (adenosine receptor blockade) administration. In protocol 2, exercise was repeated during aminophylline alone and during aminophylline-l-NMMA. Forearm vascular conductance (FVC; ml·min−1·100 mmHg−1) was calculated from blood flow (ml/min) and BAP (mmHg). Percent recovery in FVC during inflation was calculated as (steady-state inflation + exercise value − nadir)/[steady-state exercise (control) value − nadir]. In protocol 1, percent recovery in FVC was 108 ± 8% during the control (no drug) trial. Percent recovery in FVC was attenuated with inhibition of NO formation alone (78 ± 9%; P < 0.01 vs. control) and was attenuated further with combined inhibition of NO and adenosine (58 ± 9%; P < 0.01 vs. l-NMMA). In protocol 2, percent recovery was reduced with adenosine receptor blockade (74 ± 11% vs. 113 ± 6%, P < 0.01) compared with control drug trials. Percent recovery in FVC was attenuated further with combined inhibition of adenosine and NO (48 ± 11%; P < 0.05 vs. aminophylline). Our data indicate that adenosine contributes to compensatory vasodilation in an NO-independent manner during exercise with acute hypoperfusion.

Dietary salt enhances glomerular endothelial nitric oxide synthase through TGF-β1

1998 ◽  
Vol 275 (1) ◽  
pp. F18-F24 ◽  
Author(s):  
Wei-Zhong Ying ◽  
Paul W. Sanders
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Transforming Growth Factor ◽  
No Production ◽  
Dietary Salt ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Tgf Β1

Dietary salt controls production of nitric oxide (NO), a potent paracrine relaxation factor involved in glomerular filtration and salt excretion. We hypothesized that glomerular NO production was enhanced through endothelial nitric oxide synthase (NOS3). Rats in metabolic cages were studied after 4 days on 0.3% (Lo-salt) or 8.0% (Hi-salt) NaCl diet. Steady-state mRNA and protein levels of NOS3 and calcium-dependent NO production of isolated glomeruli from Hi-salt animals were greater than those values observed in glomeruli from Lo-salt rats. Because dietary salt enhanced glomerular production of transforming growth factor-β1 (TGF-β1) [W.-Z. Ying and P. W. Sanders. Am. J. Physiol. 274 ( Renal Physiol. 43): F635–F641, 1998], studies were then conducted to examine the interaction between NOS3 and TGF-β1. Glomerular steady-state levels of mRNA of NOS3 and TGF-β1 directly correlated ( r 2 = 0.946; P < 0.0001). A neutralizing antibody to TGF-β reduced NOS3 protein and NO production in cultured glomeruli from Hi-salt animals to levels seen in the Lo-salt glomeruli. Thus dietary salt increased glomerular expression of TGF-β1, which in turn augmented NO production through NOS3.

scholarly journals Nitric oxide inhibits sodium/hydrogen exchange activity in the thick ascending limb

1999 ◽  
Vol 277 (3) ◽  
pp. F377-F382 ◽  
Author(s):  
Jeffrey L. Garvin ◽  
Nancy J. Hong
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Hydrogen Exchange ◽  
Thick Ascending Limb ◽  
Acid Base Balance ◽  
No Donor ◽  
Base Balance ◽  
Dimethyl Amiloride ◽  
Oxide Synthase ◽  
Spermine Nonoate

Nitric oxide (NO) inhibits transport in various nephron segments, and the thick ascending limb (TAL) expresses nitric oxide synthase (NOS). However, the effects of NO on TAL transport have not been extensively studied. We tested the hypothesis that NO inhibits apical and basolateral Na+/H+exchange by the TAL by measuring intracellular pH (pHi) of isolated, perfused rat TALs using the fluorescent dye 2′,7′-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF). The NO donor spermine NONOate (SPM, 10 μM) decreased steady-state pHi in medullary TALs from 7.18 ± 0.13 to 7.13 ± 0.14 ( P < 0.02), whereas controls did not decrease significantly. We next measured the buffering capacity of medullary TALs and the rate at which they recovered from acid loads to investigate the mechanism whereby NO reduces steady-state pHi. SPM decreased H+ flux ( J H) from 2.41 ± 0.66 to 0.97 ± 0.19 pmol ⋅ min−1 ⋅ mm−1, 55%. To assure that the decrease in J H was due to NO, another donor, nitroglycerin (NTG; 10 μM), was used. NTG decreased J H from 1.65 ± 0.11 to 1.07 ± 0.24 pmol ⋅ min−1 ⋅ mm−1, 37%. To determine the relative contributions of the apical and basolateral Na+/H+exchangers, 5-( N, N-dimethyl)amiloride (DMA; 100 μM) was added to either bath or lumen. With DMA added to the bath, SPM decreased J H from 4.78 ± 1.08 to 2.74 ± 0.54 pmol ⋅ min−1 ⋅ mm−1, an inhibition of 41%; and with DMA added to the lumen, SPM decreased J H from 2.31 ± 0.29 to 1.74 ± 0.27 pmol ⋅ min−1 ⋅ mm−1, a reduction of 26%. Addition of DMA alone to both bath and lumen resulted in an 87% inhibition of J H. We conclude that NO inhibits both apical and basolateral Na+/H+exchangers and consequently may play an important role in regulating pHi and may alter acid/base balance by directly affecting bicarbonate absorption in the TAL.

Garlic attenuates nitric oxide production in rat cardiac myocytes through inhibition of inducible nitric oxide synthase and the arginine transporter CAT-2 (cationic amino acid transporter-2)

2002 ◽  
Vol 102 (5) ◽  
pp. 487-493 ◽  
Author(s):  
Idit F. SCHWARTZ ◽  
Rami HERSHKOVITZ ◽  
Adrian IAINA ◽  
Ehud GNESSIN ◽  
Yoram WOLLMAN ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Antioxidant Activity ◽  
Steady State ◽  
Amino Acid ◽  
Cardiac Myocytes ◽  
Inos Mrna ◽  
Mrna Levels ◽  
Cationic Amino Acid Transporter ◽  
Cationic Amino Acid ◽  
Nitrite Production

It is now accepted that allicin, the main biologically active compound in garlic, exhibits antioxidant activity. The present study was designed to test the hypothesis that the antioxidant activity of garlic can be partially attributed to the inhibition of nitric oxide (NO) production by cytokine-induced NO synthase (iNOS). Cardiac myocytes cultured from neonatal Wistar rats were stimulated by lipopolysaccharide (LPS) and incubated for 24h with various concentrations of allicin. This resulted in marked inhibition of nitrite production. Interestingly, a low concentration of allicin (10μM) was significantly more potent in abrogating the effect of LPS on nitrite production than a higher concentration (40μM). Allicin decreased steady-state iNOS mRNA levels, and this effect was maximal when a lower concentration was used (10μM compared with 40μM). In order to explore additional effects of allicin on NO generation that might counteract the effect on iNOS, we assessed the effects of higher allicin concentrations on arginine transport. Allicin inhibited the uptake of 1mM extracellular arginine in a concentration-dependent manner. The expression of the two arginine transporters that are expressed in cardiac myocytes [CAT-1 (cationic amino acid transporter-1) and CAT-2] was studied using reverse transcription-PCR. A concentration of 200μM allicin abolished the expression of CAT-2 mRNA, 100μM significantly attenuated it, whereas 50μM had no effect. Allicin had no effect on steady-state CAT-1 mRNA levels. Our results suggest that allicin inhibits iNOS activity through two different mechanisms: at lower concentrations it decreases iNOS mRNA levels, whereas at higher concentrations it inhibits arginine transport through down-regulation of CAT-2 mRNA.

scholarly journals Differences in nitric oxide steady states between arginine, hypoxanthine, uracil auxotrophs (AHU) and non-AHU strains ofNeisseria gonorrhoeaeduring anaerobic respiration in the presence of nitrite

2008 ◽  
Vol 54 (8) ◽  
pp. 639-646 ◽  
Author(s):  
Kenneth Barth ◽  
Virginia L. Clark
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Nitrite Reductase ◽  
Anaerobic Respiration ◽  
State Level ◽  
Cell Number ◽  
Steady State Level ◽  
No Donor ◽  
Membrane Function ◽  
Uracil Auxotrophs

Neisseria gonorrhoeae can grow by anaerobic respiration using nitrite as an alternative electron acceptor. Under these growth conditions, N. gonorrhoeae produces and degrades nitric oxide (NO), an important host defense molecule. Laboratory strain F62 has been shown to establish and maintain a NO steady-state level that is a function of the nitrite reductase/NO reductase ratio and is independent of cell number. The nitrite reductase activities (122–197 nmol NO2reduced·min–1·OD600–1) and NO reductase activities (88–155 nmol NO reduced·min–1·OD600–1) in a variety of gonococcal clinical isolates were similar to the specific activities seen in F62 (241 nmol NO2reduced·min–1·OD600–1and 88 nmol NO reduced·min–1·OD600–1, respectively). In seven gonococcal strains, the NO steady-state levels established in the presence of nitrite were similar to that of F62 (801–2121 nmol·L–1NO), while six of the strains, identified as arginine, hypoxanthine, and uracil auxotrophs (AHU), that cause asymptomatic infection in men had either two- to threefold (373–579 nmol·L–1NO) or about 100-fold (13–24 nmol·L–1NO) lower NO steady-state concentrations. All tested strains in the presence of a NO donor, 2,2′-(hydroxynitrosohydrazono)bis-ethanimine/NO, quickly lowered and maintained NO levels in the noninflammatory range of NO (<300 nmol·L–1). The generation of a NO steady-state concentration was directly affected by alterations in respiratory control in both F62 and an AHU strain, although differences in membrane function are suspected to be responsible for NO steady-state level differences in AHU strains.

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