Cross-Talk between the Red Blood Cell and the Endothelium: Nitric Oxide as a Paracrine and Endocrine Regulator of Vascular Tone

2010 ◽  
pp. 562-575
Author(s):  
Sruti Shiva ◽  
Mark T. Gladwin
Keyword(s):  
Nitric Oxide ◽  
Blood Cell ◽  
Cross Talk ◽  
Red Blood Cell ◽  
Vascular Tone

Nitric oxide influences red blood cell velocity independently of changes in the vascular tone

2011 ◽  
Vol 45 (6) ◽  
pp. 653-661 ◽  
Author(s):  
Patrick Horn ◽  
Miriam M. Cortese-Krott ◽  
Stefanie Keymel ◽  
Intan Kumara ◽  
Sandra Burghoff ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Vascular Tone ◽  
Cell Velocity ◽  
Red Blood Cell Velocity

scholarly journals Recent insights into nitrite signaling processes in blood

2017 ◽  
Vol 398 (3) ◽  
pp. 319-329 ◽  
Author(s):  
Christine C. Helms ◽  
Xiaohua Liu ◽  
Daniel B. Kim-Shapiro
Keyword(s):  
Nitric Oxide ◽  
Human Physiology ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Nitrite Reduction ◽  
No Production ◽  
The Past ◽  
Acidic Conditions ◽  
Hypoxic Vasodilation

Abstract Nitrite was once thought to be inert in human physiology. However, research over the past few decades has established a link between nitrite and the production of nitric oxide (NO) that is potentiated under hypoxic and acidic conditions. Under this new role nitrite acts as a storage pool for bioavailable NO. The NO so produced is likely to play important roles in decreasing platelet activation, contributing to hypoxic vasodilation and minimizing blood-cell adhesion to endothelial cells. Researchers have proposed multiple mechanisms for nitrite reduction in the blood. However, NO production in blood must somehow overcome rapid scavenging by hemoglobin in order to be effective. Here we review the role of red blood cell hemoglobin in the reduction of nitrite and present recent research into mechanisms that may allow nitric oxide and other reactive nitrogen signaling species to escape the red blood cell.

scholarly journals Analysis of nitric oxide donor effectiveness in resistance vessels

2005 ◽  
Vol 288 (5) ◽  
pp. H2390-H2399 ◽  
Author(s):  
Daniel R. Hyduke ◽  
James C. Liao
Keyword(s):  
Nitric Oxide ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Interstitial Space ◽  
The Body ◽  
Nitric Oxide Donor ◽  
Free Zone ◽  
Pathological Conditions ◽  
Resistance Vessels ◽  
No Bioavailability

Decreased nitric oxide (NO) bioavailability is associated with a number of pathological conditions. Administration of a supplemental source of NO can counter the pathological effects arising from decreased NO bioavailability. A class of NO-nucleophile adducts that spontaneously release NO (NONOates) has been developed, and its members show promise as therapeutic sources of NO. Because the NONOates release NO spontaneously, a significant portion of the NO may be consumed by the myriad of NO reactive species present in the body. Here we develop a model to analyze the efficacy of NO delivery, by membrane-impermeable NONOates, in the resistance arterioles. Our model identifies three features of blood vessels that will enhance NONOate efficacy: 1) the amount of NO delivered to the abluminal region increases with lumen radius; 2) the presence of a flow-induced red blood cell-free zone will augment NO delivery; and 3) extravasation of the NONOate into the interstitial space will increase abluminal NO delivery. These results suggest that NONOates may be more effective in larger vessels and that NONOate efficacy can be altered by modifying permeability to the interstitial space.

Modulation of endothelial nitric oxide synthase expression by red blood cell aggregation

2004 ◽  
Vol 286 (1) ◽  
pp. H222-H229 ◽  
Author(s):  
Oguz K. Baskurt ◽  
Ozlem Yalcin ◽  
Sadi Ozdem ◽  
Jonathan K. Armstrong ◽  
Herbert J. Meiselman
Keyword(s):  
Nitric Oxide ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Aggregation ◽  
Shear Stresses ◽  
Control Mechanisms ◽  
Vascular Control ◽  
Arterial Blood ◽  
Rbc Aggregation ◽  
Endothelial Nitric Oxide

The effects of enhanced red blood cell (RBC) aggregation on nitric oxide (NO)-dependent vascular control mechanisms have been investigated in a rat exchange transfusion model. RBC aggregation for cells in native plasma was increased via a novel method using RBCs covalently coated with a 13-kDa poloxamer copolymer (Pluronic F-98); control experiments used RBCs coated with a nonaggregating 8.4-kDa poloxamer (Pluronic F-68). Rats exchange transfused with aggregating RBC suspensions demonstrated significantly enhanced RBC aggregation throughout the 5-day follow-up period, with mean arterial blood pressure increasing gradually over this period. Arterial segments (≈300 μm in diameter) were isolated from gracilis muscle on the fifth day and mounted between two glass micropipettes in a special chamber equipped with pressure servo-control system. Dose-dependent dilation by ACh and flow-mediated dilation of arterial segments pressurized to 30 mmHg and preconstricted to 45–55% of the original diameter by phenylephrine were significantly blunted in rats with enhanced RBC aggregation. Both responses were totally abolished by nonspecific NO synthase (NOS) inhibitor ( Nω-nitro-l-arginine methyl ester) treatment of arterial segments, indicating that the responses were NO related. Additionally, expression of endothelial NOS protein was found to be decreased in muscle samples obtained from rats exchanged with aggregating cell suspensions. These results imply that enhanced RBC aggregation results in suppressed expression of NO synthesizing mechanisms, thereby leading to altered vasomotor tonus; the mechanisms involved most likely relate to decreased wall shear stresses due to decreased blood flow and/or increased axial accumulation of RBCs.

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