scholarly journals PO-277 Nitric oxide generation in red blood cells induced by exercise

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Zhenghui Zha ◽  
Yuli Zhang
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Red Blood Cells ◽  
Blood Vessels ◽  
Blood Cells ◽  
White Blood Cells ◽  
Pi3k Pathway ◽  
No Production ◽  
Hemodynamic Changes ◽  
Enzyme Source

Objective Vascular endothelial nitric oxide synthase (NOS) is considered to be the main enzyme source for NO production in blood vessels, and studies have shown that RBC may also express NOS and produce NO. The purpose of this study was to summarize the expression of NOS in vascular red blood cells caused by changes in hemodynamics, and to improve the bioavailability of NO, and to lay a theoretical foundation for exploring the mechanism of exercise to improve vasodilation. Methods A literature review method was used to analyze related studies on exercise and RBC-NOS published in recent years. Results Intravascular NO is one of the most important vascular signaling molecules, which has the function of relaxing blood vessels. NO is produced during the conversion of L-arginine into L-citrulline, which is mainly dependent on the regulation of vascular eNOS. RBC can express NOS under certain action, and RBC-NOS is mainly located on RBC membrane and cytoplasm; The regulatory mechanisms of RBC-NOS and eNOS have similarities and differences: RBC-NOS and eNOS are both dependent on Ca2+ regulation and phosphorylation of Serine 1177  via the PI3K pathway; however, since red blood cells do not have nuclei, endoplasmic reticulum and Golgi, they do not have other mechanisms of action of eNOS. Therefore, the vascular endothelium is not the only source of NO production. Red blood cells, white blood cells and platelets can produce NO. The amount of NO produced by red blood cells is significantly higher than that of white blood cells and platelets，it is another major source of NO production in blood vessels.The level of wall shear stress is the main determinant of NOS expression in blood vessels: On the one hand, exercise training can cause hemodynamic changes, increased shear stress, and induce changes in eNOS and RBC-NOS levels, increase NO bioavailability, and participate in the regulation of vasodilation.On the other hand, moderate-intensity exercise causes NO produced by RBC to increase red blood cell deformability and participate in vascular regulation. Conclusions 1.Erythrocyte is an enzyme source that relies on hemodynamics to release NO from the blood vessel wall. It is regulated by Ca2+ and phosphorylates ser1177 through the PI3K pathway to participate in the regulation of the body. 2.Hemodynamic changes caused by exercise training can simultaneously induce the expression of eNOS and RBC-NOS, increase the bioavailability of NO, and jointly mediate vasodilation.

Shear-stress mediated nitric oxide production within red blood cells: A dose-response

2019 ◽  
Vol 71 (2) ◽  
pp. 203-214 ◽  
Author(s):  
Jarod T. Horobin ◽  
Nobuo Watanabe ◽  
Masaya Hakozaki ◽  
Surendran Sabapathy ◽  
Michael J. Simmonds
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Red Blood Cells ◽  
Dose Response ◽  
Blood Cells ◽  
Nitric Oxide Production ◽  
Oxide Production

scholarly journals Shear stress activation of nitric oxide synthase and increased nitric oxide levels in human red blood cells

Nitric Oxide ◽  
2011 ◽  
Vol 24 (4) ◽  
pp. 184-191 ◽  
Author(s):  
Pinar Ulker ◽  
Nazmi Yaras ◽  
Ozlem Yalcin ◽  
Ciler Celik-Ozenci ◽  
Paul C. Johnson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Shear Stress ◽  
Nitric Oxide Synthase ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Human Red Blood Cells ◽  
Oxide Synthase ◽  
Stress Activation

Prolongation of bleeding time by acute hemolysis in rats: a role for nitric oxide

1997 ◽  
Vol 272 (6) ◽  
pp. H2875-H2884 ◽  
Author(s):  
T. Wollny ◽  
L. Iacoviello ◽  
W. Buczko ◽  
G. de Gaetano ◽  
M. B. Donati
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Blood Cell ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Adhesion ◽  
Bleeding Time ◽  
Ex Vivo ◽  
White Blood Cells

The present study was aimed at clarifying the interaction between red blood cell trauma and bleeding observed in some clinical conditions. Acute hemolysis provoked by distilled water injection was followed by a significant prolongation of the "template" bleeding time in rats. Comparable effects were observed after injection of an isotonic lysate of washed red blood cells. N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) formation from L-arginine, normalized bleeding time when given to rats before hemolysis induction. The occurrence of hemolysis decreased ex vivo platelet adhesion to collagen without affecting platelet aggregation and induced a transient drop in blood pressure, the latter occurring during the first minute after injection. L-NAME pretreatment increased ex vivo platelet adhesion but did not affect either platelet aggregation or fall in blood pressure. All the effects of L-NAME were blunted by treating the animals with the NO precursor L-arginine but not D-arginine. Incubation of the erythrocyte lysate with apyrase prevented the prolongation of bleeding time induced by the hemolysate. Moreover, ADP administration, at doses that did not increase hemoglobin levels, induced effects similar to those observed after hemolysis (on template bleeding time and ex vivo platelet adhesion), which were also reversed by L-NAME and restored by L-arginine. ADP is abundantly released from (hemo)lysed red blood cells and is known to stimulate release of NO, a potent vasodilator and inhibitor of platelet adhesion. ADP-dependent NO release could be responsible for bleeding time prolongation, due to abnormalities in platelet-vessel wall interaction, during acute hemolysis. Lysis of white blood cells may also contribute to prolongation of bleeding time. Because ADP could not be detected in these cells, we postulate that other mechanisms also can be involved in bleeding time prolongation after blood cell activation in vivo.

scholarly journals Mature Twin Neonates Exhibit Oxidative Stress via Nitric Oxide Synthase Dysfunctionality: A Prognostic Stress Marker in the Red Blood Cells and Umbilical Cord Vessels

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 845
Author(s):  
Payal Chakraborty ◽  
Krisztina N. Dugmonits ◽  
Hajnalka Orvos ◽  
Edit Hermesz
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Red Blood Cells ◽  
Umbilical Cord ◽  
Blood Cells ◽  
Low Birthweight ◽  
Multiple Pregnancy ◽  
No Production ◽  
Oxide Synthase

Intrauterine hypoxic condition increases the generation of reactive oxygen species and fetal oxidative stress. Multiple pregnancy always bears an additional oxidative stress condition with severe complications, such as prematurity, structural abnormalities, delayed development and low birthweight. The umbilical cord (UC) vessels, along with circulating fetal red blood cells (RBCs), highly determine the oxygenation status of fetus and regulate the feto-placental circulation. As UC lacks innervation, the activation of the endothelial nitric oxide synthase (NOS3) is fundamental for proper NO production. Therefore, we aimed to study the NOS3 activation pathways along with damages to macromolecules in the endothelium of UC vessels and RBCs of mature non-discordant twins, in connection to major differences in their birth weight. We provide evidence that, under severe hypoxic conditions such as twin pregnancy, the NOS3-related NO production pathways are altered both in UC vessels and RBCs; moreover, the extent of changes is highly birthweight-specific. Furthermore, macromolecular damages are prominent in the RBCs and arteries compared to the vein, with a similar increase in the Arginase1 level, which is believed to play a role in NOS3 functionality, resulting in endothelial dysfunctionality, which might have relevance to the major etiologies of cardiovascular diseases in later life.

Brisk production of nitric oxide and associated formation of S-nitrosothiols in early hemorrhage

2006 ◽  
Vol 100 (4) ◽  
pp. 1267-1277 ◽  
Author(s):  
James L. Atkins ◽  
Billy W. Day ◽  
Michael T. Handrigan ◽  
Zhe Zhang ◽  
Motilal B. Pamnani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electron Paramagnetic Resonance ◽  
Red Blood Cells ◽  
Blood Cells ◽  
No Synthase ◽  
Resonance Spectroscopy ◽  
No Production ◽  
Paramagnetic Resonance ◽  
Arterial Blood ◽  
Electron Paramagnetic

The results of previous inhibitor studies suggest that there is some increase in nitric oxide (NO) production from constitutive NO synthase in early hemorrhage (H), but the magnitude of NO production early after H has not been previously assessed. It is generally believed that only modest production rates are possible from the constitutively expressed NO synthases. To study this, anesthetized male Sprague-Dawley rats were subjected to 90 min of isobaric (40 mmHg) H. During this period of time, the dynamics of accumulation of NO intermediates in the arterial blood was assessed using electron paramagnetic resonance spectroscopy, chemiluminescence, fluorescence imaging, and mass spectrometry. Electron paramagnetic resonance-detectable NO adducts were also measured with spin traps in blood plasma and red blood cells. H led to an increase in the concentration of hemoglobin-NO from 0.9 ± 0.2 to 4.8 ± 0.7 μM. This accumulation was attenuated by a nonselective inhibitor of NO synthase, NG-nitro-l-argininemethyl ester (l-NAME), but not by NG-nitro-d-argininemethyl ester (d-NAME) or 1400W. Administration of l-NAME (but not 1400W or d-NAME) during H produced a short-term increase in mean arterial pressure (∼90%). In H, the level of N oxides in red blood cells increased sevenfold. S-nitrosylation of plasma proteins was revealed with “biotin switch” techniques. The results provide compelling evidence that there is brisk production of NO in early H. The results indicate that the initial compensatory response to H is more complicated than previously realized, and it involves an orchestrated balance between intense vasoconstrictor and vasodilatory components.

scholarly journals Maternal Smoking Highly Affects the Function, Membrane Integrity, and Rheological Properties in Fetal Red Blood Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Krisztina N. Dugmonits ◽  
Payal Chakraborty ◽  
Réka Hollandi ◽  
Szabolcs Zahorán ◽  
Gabriella Pankotai-Bodó ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Maternal Smoking ◽  
Vascular Dysfunction ◽  
Membrane Integrity ◽  
No Production ◽  
Detailed Knowledge ◽  
Heavy Smoking ◽  
Wide Range

An understanding of the basic pathophysiological mechanisms of neonatal diseases necessitates detailed knowledge about the wide range of complications in the circulating fetal RBCs. Recent publications on adult red blood cells (RBCs) provide evidence that RBCs carry an active nitric oxide synthase (NOS3) enzyme and contribute to vascular functioning and integrity via their active nitric oxide synthesis. The aim of this study was to determine the effect of maternal smoking on the phenotypical appearance and functionality of fetal RBCs, based on morphological and molecular studies. We looked for possible links between vascular dysfunction and NOS3 expression and activation and its regulation by arginase (ARG1). Significant morphological and functional differences were found between fetal RBCs isolated from the arterial cord blood of neonates born to nonsmoking (RBC-NS, n=62) and heavy-smoking (RBC-S, n=51) mothers. Morphological variations were quantified by Advanced Cell Classifier, microscopy-based intelligent analysis software. To investigate the relevance of the newly suggested “erythrocrine” function in fetal RBCs, we measured the levels of NOS3 and its phosphorylation in parallel with the level of ARG1, as one of the major influencers of NOS3 dimerization, by fluorescence-activated cell sorting. Fetal RBCs, even the “healthy-looking” biconcave-shaped type, exhibited impaired NOS3 activation in the RBC-S population, which was paralleled with elevated ARG1 level, thus suggesting an increased redox burden. Our molecular data indicate that maternal smoking can exert marked effects on the circulating fetal RBCs, which could have a consequence on the outcome of in utero development. We hypothesize that any endothelial dysfunction altering NO production/bioavailability can be sensed by circulating fetal RBCs. Hence, we are putting forward the idea that neonatal RBC could serve as a real-time sensor for not only monitoring RBC-linked anomalies but also predicting the overall status of the vascular microenvironment.

Hemoglobin and red blood cells alter the response of expired nitric oxide to mechanical forces

2000 ◽  
Vol 279 (6) ◽  
pp. H2947-H2953 ◽  
Author(s):  
John T. Berg ◽  
Steven Deem ◽  
Mark E. Kerr ◽  
Erik R. Swenson
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Venous Pressure ◽  
No Production ◽  
Mechanical Forces ◽  
Blood Flow Reduction ◽  
Lung Epithelial ◽  
Isolated Lungs

Expired nitric oxide (NOe) varies with hemodynamic or ventilatory perturbations, possibly due to shear stress- or stretch-stimulated NO production. Since hemoglobin (Hb) binds NO, NOe changes may reflect changes in blood volume and flow. To determine the role of blood and mechanical forces, we measured NOe in anesthetized rabbits, as well as rabbit lungs perfused with buffer, red blood cells (RBCs) or Hb following changes in flow, venous pressure (Pv), and positive end-expiratory pressure (PEEP). In buffer-perfused lungs decreases in flow and Pv reduced NOe, but NOe rose when RBCs and Hb were present. These findings are consistent with changes in vascular NO production, whose detection is obscured in blood-perfused lungs by the more dominant effect of Hb NO scavenging. PEEP decreased NOe in all perfused lungs but increased NOe in live rabbits. The NOe fall with PEEP in isolated lungs is consistent with flow redistribution from alveolar septal capillaries to extra-alveolar vessels and decreased surface area or a direct, stretch-mediated depression of lung epithelial NO production. In live rabbits, increased NOe may reflect blood flow reduction and decreased Hb NO scavenging and/or autonomic responses that increase NO production. We conclude that blood and systemic responses render it difficult to use NOe changes as an accurate measure of lung tissue NO production.

The Effect of Red Blood Cells on the ADP-induced Aggregation of Human Platelets in Flow Through Tubes

1990 ◽  
Vol 63 (01) ◽  
pp. 112-121 ◽  
Author(s):  
David N Bell ◽  
Samira Spain ◽  
Harry L Goldsmith
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Platelet Rich Plasma ◽  
Mean Transit Time ◽  
White Blood Cells ◽  
Aggregate Size ◽  
Human Platelets ◽  
Induced Aggregation

SummaryThe effect of red blood cells, rbc, and shear rate on the ADPinduced aggregation of platelets in whole blood, WB, flowing through polyethylene tubing was studied using a previously described technique (1). Effluent WB was collected into 0.5% glutaraldehyde and the red blood cells removed by centrifugation through Percoll. At 23°C the rate of single platelet aggregtion was upt to 9× greater in WB than previously found in platelet-rich plasma (2) at mean tube shear rates Ḡ = 41.9,335, and 1,920 s−1, and at both 0.2 and 1.0 µM ADP. At 0.2 pM ADP, the rate of aggregation was greatest at Ḡ = 41.9 s−1 over the first 1.7 s mean transit time through the flow tube, t, but decreased steadily with time. At Ḡ ≥335 s−1 the rate of aggregation increased between t = 1.7 and 8.6 s; however, aggregate size decreased with increasing shear rate. At 1.0 µM ADP, the initial rate of single platelet aggregation was still highest at Ḡ = 41.9 s1 where large aggregates up to several millimeters in diameter containing rbc formed by t = 43 s. At this ADP concentration, aggregate size was still limited at Ḡ ≥335 s−1 but the rate of single platelet aggregation was markedly greater than at 0.2 pM ADP. By t = 43 s, no single platelets remained and rbc were not incorporated into aggregates. Although aggregate size increased slowly, large aggregates eventually formed. White blood cells were not significantly incorporated into aggregates at any shear rate or ADP concentration. Since the present technique did not induce platelet thromboxane A2 formation or cause cell lysis, these experiments provide evidence for a purely mechanical effect of rbc in augmenting platelet aggregation in WB.

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