Cited by 309Blood properties and coagulationNitric Oxide and Endothelin EffectsErythrocyte Function and Pathophysiology

Effects of nitric oxide on red blood cell deformability

Bor-Kucukatay, Melek, Wenby, Rosalinda B., Meiselman, Herbert J., Baskurt, Oguz K.·2003·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

In addition to its known action on vascular smooth muscle, nitric oxide (NO) has been suggested to have cardiovascular effects via regulation of red blood cell (RBC) deformability. The present study was designed to further explore this possibility. Human RBCs in autologous plasma were incubated for 1 h with NO synthase (NOS) inhibitors [ N ω-nitro-l-arginine methyl ester (l-NAME) and S-methylisothiourea], NO donors [sodium nitroprusside (SNP) and diethylenetriamine (DETA)-NONOate], an NO precursor (l-arginine), soluble guanylate cyclase inhibitors (1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one and methylene blue), and a potassium channel blocker [triethylammonium (TEA)]. After incubation, RBC deformability at various shear stresses was determined by ektacytometry. Both NOS inhibitors significantly reduced RBC deformability above a threshold concentration, whereas the NO donors increased deformability at optimal concentrations. NO donors, as well as the NO precursor l-arginine and the potassium blocker TEA, were able to reverse the effects of NOS inhibitors. Guanylate cyclase inhibition reduced RBC deformation, with both SNP and DETA-NONOate able to reverse this effect. These results thus indicate the importance of NO as a determinant of RBC mechanical behavior and suggest its regulatory role for normal RBC deformability.

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Crossref · 10.1152/ajpheart.00665.2002

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Authors
Bor-Kucukatay, M., Wenby, R. B., Meiselman, H. J., & Baskurt, O. K.
Affiliations
  • Department of Physiology, Faculty of Medicine, Akdeniz University, Antalya, 07070 Turkey; and
  • Department of Physiology and Biophysics, Keck School of Medicine, Los Angeles, California 90033
  • Akdeniz University (TR)
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2003-05-01
Volume
284
Issue
5
Pages
H1577-H1584
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2096465912
Cited by
309
References
46
Citations by year
2026: 4 · 2025: 8 · 2024: 19 · 2023: 13 · 2022: 16 · 2021: 11 · 2020: 11 · 2019: 25 · 2018: 20 · 2017: 13 · 2016: 17 · 2015: 20 · 2014: 19 · 2013: 15 · 2012: 18
FWCI
6.75
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p60hl048484-10)
  • National Heart, Lung, and Blood Institute (HL48484, HL 15722)
  • Fogarty International Center (1R03 TW 01295, R03TW001295)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
Keywords
nitric oxide, erythrocyte deformability, nitric oxide synthase inhibitors, nitric oxide donors, sodium nitroprusside, DETA NONOate, L-arginine, soluble guanylate cyclase, guanylate cyclase inhibitor, potassium channel blockade, shear stress, ektacytometry, red blood cell mechanics
MeSH terms
Soluble Guanylyl Cyclase, Adult, Arginine, Calcium, Drug Interactions, Enzyme Inhibitors, Erythrocyte Deformability, Erythrocytes, Cyclic GMP, Guanylate Cyclase, Humans, Hydrazines, Male, Nitric Oxide, Nitroprusside, Nitroso Compounds, Stress, Mechanical, Hemorheology, Receptors, Cytoplasmic and Nuclear, Nitric Oxide Synthase, NG-Nitroarginine Methyl Ester, Tetraethylammonium, Nitric Oxide Donors, Potassium Channel Blockers, Cell Size

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