scholarly journals A system for exposing molecules and cells to biologically relevant and accurately controlled steady-state concentrations of nitric oxide and oxygen

Nitric Oxide ◽  
2012 ◽  
Vol 27 (3) ◽  
pp. 161-168 ◽  
Author(s):  
Vasileios Dendroulakis ◽  
Brandon S. Russell ◽  
C. Eric Elmquist ◽  
Laura J. Trudel ◽  
Gerald N. Wogan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Biologically Relevant

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.

Photoformation rate, steady-state concentration and lifetime of nitric oxide radical (NO ) in a eutrophic river in Higashi-Hiroshima, Japan

Chemosphere ◽  
2015 ◽  
Vol 119 ◽  
pp. 302-309 ◽  
Author(s):  
Adebanjo Jacob Anifowose ◽  
Kazuhiko Takeda ◽  
Hiroshi Sakugawa
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Steady State Concentration ◽  
Nitric Oxide Radical ◽  
State Concentration ◽  
Eutrophic River

Reaction between nitric oxide and ammonia on polycrystalline platinum. 1. Steady-state kinetics

1983 ◽  
Vol 87 (6) ◽  
pp. 958-963 ◽  
Author(s):  
C. G. Takoudis ◽  
L. D. Schmidt
Keyword(s):  
Nitric Oxide ◽  
Steady State ◽  
Polycrystalline Platinum ◽  
Steady State Kinetics

Tyrosine confounds oxidative electrochemical detection of nitric oxide

1998 ◽  
Vol 274 (5) ◽  
pp. H1698-H1704 ◽  
Author(s):  
R. Stingele ◽  
D. A. Wilson ◽  
R. J. Traystman ◽  
D. F. Hanley
Keyword(s):  
Nitric Oxide ◽  
Blood Brain Barrier ◽  
Electrochemical Detection ◽  
Concentration Gradient ◽  
Brain Barrier ◽  
Future Studies ◽  
Biologically Relevant ◽  
Blood Brain ◽  
Dog Brain ◽  
Order Of Magnitude

We report evidence that a porphyrinic microsensor for detection of nitric oxide (NO) also detects biologically relevant concentrations of tyrosine (Tyr) in dog brain. Tyr is oxidized by this sensor at the same potential as NO, and the sensitivity for NO and Tyr are of the same order of magnitude. The interference from Tyr is of importance because 1) Tyr is abundant and 2) there is a concentration gradient of Tyr across the blood-brain barrier that can lead to unpredictable results if disturbed by ischemia or hypoxia. The knowledge of this interference is important for the interpretation of results obtained with this sensor and for the design of future studies.

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.

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