Effects of nitric oxide on red blood cell deformability.
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.
Bor-Kucukatay
Melek
M
Department of Physiology, Faculty of Medicine, Akdeniz University, Antalya, 07070 Turkey.
Wenby
Rosalinda B
RB
Meiselman
Herbert J
HJ
Baskurt
Oguz K
OK
D000328:Adult; D001120:Arginine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D048429:Cell Size / Q000187:drug effects; D006152:Cyclic GMP / Q000378:metabolism; D004347:Drug Interactions; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004907:Erythrocyte Deformability / Q000187:drug effects / Q000502:physiology*; D004912:Erythrocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006162:Guanylate Cyclase; D018056:Hemorheology; D006801:Humans; D006834:Hydrazines / Q000494:pharmacology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D009603:Nitroso Compounds; D026902:Potassium Channel Blockers / Q000494:pharmacology; D018160:Receptors, Cytoplasmic and Nuclear / Q000037:antagonists & inhibitors; D000071756:Soluble Guanylyl Cyclase; D013314:Stress, Mechanical; D019789:Tetraethylammonium / Q000494:pharmacology
D004791:Enzyme Inhibitors; D006834:Hydrazines; D020030:Nitric Oxide Donors; D009603:Nitroso Compounds; D026902:Potassium Channel Blockers; D018160:Receptors, Cytoplasmic and Nuclear; C094210:2,2'-(hydroxynitrosohydrazono)bis-ethanamine; D009599:Nitroprusside; D009569:Nitric Oxide; D019789:Tetraethylammonium; D001120:Arginine; D019001:Nitric Oxide Synthase; D006162:Guanylate Cyclase; D000071756:Soluble Guanylyl Cyclase; D006152:Cyclic GMP; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester