Role of cardiopulmonary bypass and cardioplegic arrest in the regulation of cardiac nitric oxide synthase activity

2002 ◽  
Vol 124 (2) ◽  
pp. 418-419 ◽  
Author(s):  
Uwe Mehlhorn ◽  
Wilhelm Bloch
Keyword(s):  
Nitric Oxide ◽  
Cardiopulmonary Bypass ◽  
Nitric Oxide Synthase ◽  
Cardioplegic Arrest ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

scholarly journals eNOS activation and NO function: Structural motifs responsible for the posttranslational control of endothelial nitric oxide synthase activity

2011 ◽  
Vol 210 (3) ◽  
pp. 271-284 ◽  
Author(s):  
Ruslan Rafikov ◽  
Fabio V Fonseca ◽  
Sanjiv Kumar ◽  
Daniel Pardo ◽  
Charles Darragh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Posttranslational Modifications ◽  
Endothelial Nitric Oxide Synthase ◽  
Regulatory Region ◽  
Enos Uncoupling ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Nitric Oxide Synthase Activity

Rather than being a constitutive enzyme as was first suggested, endothelial nitric oxide synthase (eNOS) is dynamically regulated at the transcriptional, posttranscriptional, and posttranslational levels. This review will focus on how changes in eNOS function are conferred by various posttranslational modifications. The latest knowledge regarding eNOS targeting to the plasma membrane will be discussed as the role of protein phosphorylation as a modulator of catalytic activity. Furthermore, new data are presented that provide novel insights into how disruption of the eNOS dimer prevents eNOS uncoupling and the production of superoxide under conditions of elevated oxidative stress and identifies a novel regulatory region we have termed the ‘flexible arm’.

scholarly journals Inhibition of MEK/ERK1/2 signalling alters endothelial nitric oxide synthase activity in an agonist-dependent manner

2006 ◽  
Vol 398 (2) ◽  
pp. 279-288 ◽  
Author(s):  
Jacqueline M. Cale ◽  
Ian M. Bird
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Intracellular Trafficking ◽  
Enos Activity ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Nitric Oxide Synthase Activity

eNOS (endothelial nitric oxide synthase) activity is post-translationally regulated in a complex fashion by acylation, protein–protein interactions, intracellular trafficking and phosphorylation, among others. Signalling pathways that regulate eNOS activity include phosphoinositide 3-kinase/Akt, cyclic nucleotide-dependent kinases [PKA (protein kinase A) and PKG], PKC, as well as ERKs (extracellular-signal-regulated kinases). The role of ERKs in eNOS activation remains controversial. In the present study, we have examined the role of ERK1/2 in eNOS activation in HUVEC-CS [transformed HUVEC (human umbilical-vein endothelial cells)] as well as a widely used model for eNOS study, transiently transfected COS-7 cells. U0126 pretreatment of HUVEC-CS potentiated ATP-stimulated eNOS activity, independent of changes in intracellular Ca2+ concentration ([Ca2+]i). In COS-7 cells transiently expressing ovine eNOS, U0126 potentiated A23187-stimulated eNOS activity, but inhibited ATP-stimulated activity. Compensatory changes in phosphorylation of five key eNOS residues did not account for changes in A23187-stimulated activity. However, in the case of ATP, altered phosphorylation and changes in [Ca2+]i may partially contribute to U0126 inhibition of activity. Finally, seven eNOS alanine mutants of putative ERK1/2 targets were generated and the effects of U0126 pretreatment on eNOS activity were gauged with A23187 and ATP treatment. T97A-eNOS was the only construct significantly different from wild-type after U0126 pretreatment and ATP stimulation of eNOS activation. In the present study, eNOS activity was either potentiated or inhibited in COS-7 cells, suggesting agonist dependence for MEK/ERK1/2 signalling [where MEK is MAPK (mitogen-activated protein kinase)/ERK kinase] to eNOS and a complex mechanism including [Ca2+]i, phosphorylation and, possibly, intracellular trafficking.

Role of dietary fish oil on nitric oxide synthase activity and oxidative status in mice red blood cells

2014 ◽  
Vol 5 (12) ◽  
pp. 3208-3215 ◽  
Author(s):  
Marcela A. Martins ◽  
Monique B. Moss ◽  
Iara K. S. Mendes ◽  
Márcia B. Águila ◽  
Carlos Alberto Mandarim-de-Lacerda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fatty Acids ◽  
Nitric Oxide Synthase ◽  
Fish Oil ◽  
Blood Cells ◽  
Oxidative Status ◽  
Dietary Fish ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

The consumption of n-3 polyunsaturated fatty acids derived from fish oil is associated with cardiovascular benefits, which may result from the participation of nitric oxide.

Reduction of Placental Nitric Oxide Synthase Activity in Pre-Eclampsia

1997 ◽  
Vol 93 (1) ◽  
pp. 51-55 ◽  
Author(s):  
S. P. Brennecke ◽  
N. M. Gude ◽  
J. L. Di Iulio ◽  
R. G. King
Keyword(s):  
Nitric Oxide ◽  
Adverse Effect ◽  
Nitric Oxide Synthase ◽  
Mode Of Delivery ◽  
Placental Tissue ◽  
Potent Vasodilator ◽  
Tissue Homogenates ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

1. The role of the potent vasodilator nitric oxide in the pathogenesis of pre-eclampsia is unclear. We have tested the hypothesis that placental activity of the enzyme which synthesizes nitric oxide (nitric oxide synthase) is reduced in pre-eclampsia. 2. Placentae were obtained after vaginal delivery or Caesarean section from women who had been assigned to the following groups according to standard obstetric criteria: term non-pre-eclamptic control, term pre-eclamptic, preterm non-pre-eclamptic control and preterm pre-eclamptic. Nitric oxide synthase activity of placental tissue homogenates was assessed by measuring conversion of [3H]l-arginine into [3H]l-citrulline in the presence of NADPH, FAD, tetrahydrobiopterin, calmodulin, CaCl2, magnesium acetate and a range of l-arginine concentrations. Michaelis Menton constants (Km) amd maximum velocities of reaction (Vmax) were calculated using Lineweaver—Burk analysis. 3. Vmax was significantly reduced in both term and preterm pre-eclamptic placentae compared with placentae from corresponding gestation-matched controls. There were no significant differences in the Km values for nitric oxide synthase between any of the four groups, nor were Vmax or Km values significantly influenced by mode of delivery. 4. These results provide evidence that human placental nitric oxide synthase activity is significantly reduced in pre-eclampsia. Such a reduction was evident at both term and preterm gestations. Reduced placental nitric oxide synthase activity may have an adverse effect on placental haemodynamic function in pre-eclampsia, and could be involved in the pathogenesis of this important and common obstetric complication.

Nitric Oxide Synthase Activity is Increased in Patients with Sepsis Syndrome

1995 ◽  
Vol 88 (2) ◽  
pp. 131-133 ◽  
Author(s):  
Helen F. Goode ◽  
Peter D. Howdle ◽  
Barry E. Walker ◽  
Nigel R. Webster
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Healthy Subjects ◽  
Sepsis Syndrome ◽  
Cell Protein ◽  
Polymorphonuclear Leucocytes ◽  
Organ Failures ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

1. We measured nitric oxide synthase activity in peripheral blood polymorphonuclear leucocytes from 10 patients with sepsis syndrome and 10 healthy subjects. 2. Synthase activity was significantly higher in patients with sepsis than in control subjects (1202 ± 579 compared with 595 ± 544 pmol of nitric oxide min−1 mg−1 of cell protein, P < 0.05). 3. Activity was greatest in those patients with the larger number of organ failures, although this failed to reach significance (1489 ± 560 in patients with three or more organ failures and 843 ± 404 pmol of nitric oxide min−1 mg−1 of cell protein in those with less than three, P = 0.11). 4. This study provides evidence for the role of overproduction of the vasodilator nitric oxide in sepsis syndrome.

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