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Effects of nitric oxide on red blood cell deformability.
Am J Physiol Heart Circ Physiol. 2003 May; 284(5):H1577-84.AJ

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(omega)-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.

Authors+Show Affiliations

Bor-Kucukatay M
Department of Physiology, Faculty of Medicine, Akdeniz University, Antalya, 07070 Turkey.
Wenby RB
No affiliation info available
Meiselman HJ
No affiliation info available
Baskurt OK
No affiliation info available

MeSH

AdultArginineCalciumCell SizeCyclic GMPDrug InteractionsEnzyme InhibitorsErythrocyte DeformabilityErythrocytesGuanylate CyclaseHemorheologyHumansHydrazinesMaleNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitroprussideNitroso CompoundsPotassium Channel BlockersReceptors, Cytoplasmic and NuclearSoluble Guanylyl CyclaseStress, MechanicalTetraethylammonium

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12521942

Citation

Bor-Kucukatay, Melek, et al. "Effects of Nitric Oxide On Red Blood Cell Deformability." American Journal of Physiology. Heart and Circulatory Physiology, vol. 284, no. 5, 2003, pp. H1577-84.
Bor-Kucukatay M, Wenby RB, Meiselman HJ, et al. Effects of nitric oxide on red blood cell deformability. Am J Physiol Heart Circ Physiol. 2003;284(5):H1577-84.
Bor-Kucukatay, M., Wenby, R. B., Meiselman, H. J., & Baskurt, O. K. (2003). Effects of nitric oxide on red blood cell deformability. American Journal of Physiology. Heart and Circulatory Physiology, 284(5), H1577-84.
Bor-Kucukatay M, et al. Effects of Nitric Oxide On Red Blood Cell Deformability. Am J Physiol Heart Circ Physiol. 2003;284(5):H1577-84. PubMed PMID: 12521942.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of nitric oxide on red blood cell deformability. AU - Bor-Kucukatay,Melek, AU - Wenby,Rosalinda B, AU - Meiselman,Herbert J, AU - Baskurt,Oguz K, Y1 - 2003/01/09/ PY - 2003/1/11/pubmed PY - 2003/5/16/medline PY - 2003/1/11/entrez SP - H1577 EP - 84 JF - American journal of physiology. Heart and circulatory physiology JO - Am J Physiol Heart Circ Physiol VL - 284 IS - 5 N2 - 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(omega)-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. SN - 0363-6135 UR - https://www.unboundmedicine.com/medline/citation/12521942/Effects_of_nitric_oxide_on_red_blood_cell_deformability_ DB - PRIME DP - Unbound Medicine ER -