Red blood cells express a functional endothelial nitric oxide synthase.

@article{Kleinbongard2006RedBC,
  title={Red blood cells express a functional endothelial nitric oxide synthase.},
  author={Petra Kleinbongard and Rainer Schulz and Tienush Rassaf and Thomas W Lauer and Andr{\'e} Dejam and Thomas Walter Jax and Intan Fatah Kumara and Putrika Prastuti Ratna Gharini and Svetlana A. Kabanova and Burcin Oz{\"u}yaman and H. G. Schn{\"u}rch and Axel G{\"o}decke and Artur Aron Weber and Mirko J. Robenek and Horst Robenek and Wilhelm Bloch and Peter R{\"o}sen and Malte Kelm},
  journal={Blood},
  year={2006},
  volume={107 7},
  pages={
          2943-51
        }
}
The synthesis of nitric oxide (NO) in the circulation has been attributed exclusively to the vascular endothelium. Red blood cells (RBCs) have been demonstrated to carry a nonfunctional NO synthase (NOS) and, due to their huge hemoglobin content, have been assumed to metabolize large quantities of NO. More recently, however, RBCs have been identified to reversibly bind, transport, and release NO within the cardiovascular system. We now provide evidence that RBCs from humans express an active… 

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References

SHOWING 1-10 OF 83 REFERENCES

Normal circulating adult human red blood cells contain inactive NOS proteins.

Findings indicate that human RBCs collected from normal adult individuals possess proteins that react with monoclonal antibodies to the Inducible and endothelial isoforms of NOS, but the proteins are without catalytic activity.

Modulation of nitric oxide bioavailability by erythrocytes

  • Kuang-Tse HuangT. H. Han J. Liao
  • Biology, Environmental Science
    Proceedings of the National Academy of Sciences of the United States of America
  • 2001
It is suggested that RBC membrane and cytoskeleton associated NO-inert proteins provide a barrier for NO diffusion and thus account for the reduction in the NO uptake rate of RBCs.

Intravascular flow decreases erythrocyte consumption of nitric oxide.

It is shown that physiological concentrations of RBCs in the presence of intravascular flow does not inhibit NO-mediated vessel dilation, suggesting that R BCs under this condition are not an NO scavenger.

Emerging role of nitrite in human biology.

Evidence for the presence of L-arginine-nitric oxide pathway in human red blood cells: relevance in the effects of red blood cells on platelet function.

Observations suggest that RBCs possess endothelium-type NO synthase and may regulate platelet function at least in part by in situ release of NO.

Nitric Oxide in the Vasculature: Physiology and Pathophysiology

  • S. Moncada
  • Biology, Medicine
    Annals of the New York Academy of Sciences
  • 1997
This deceptively simple gaseous molecule performs a wide variety of physiological functions and is likely to have a role in non-specific immunity.

Regulation of nitric oxide consumption by hypoxic red blood cells

  • T. H. HanE. Qamirani J. Liao
  • Medicine, Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 2003
It is demonstrated that under hypoxic conditions, NO accelerates its own consumption by increasing its entry into RBCs, and this phenomenon may be an evolved mechanism to stabilize the vasculature in sepsis.

Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation

It is demonstrated that the serine/threonine protein kinase Akt/PKB mediates the activation of eNOS, leading to increased NO production, and represents a novel Ca2+-independent regulatory mechanism for activation ofeNOS.

Erythrocytes Possess an Intrinsic Barrier to Nitric Oxide Consumption*

A competition test, which allows the extracellular diffusion limitation to be distinguished from transmembrane or intracellular resistance, exploited the competition between free Hb and RBCs for NO generated in a homogenous phase by an NO donor, suggesting that intrinsic RBC factors exist to reduce the NO consumption by R BCs.
...