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Am J Physiol Heart Circ Physiol (January 9, 2003). doi:10.1152/ajpheart.00665.2002
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Submitted on July 30, 2002
Accepted on January 2, 2003

The effects of nitric oxide on red blood cell deformability

Melek Bor-Kucukatay1, Rosalinda B. Wenby2, Herbert J. Meiselman2, and Oguz K. Baskurt1*

1 Department of Physiology, Akdeniz University Faculty of Medicine, Antalya, Turkey
2 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: baskurt{at}akdeniz.edu.tr.

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 RBC in autologous plasma were incubated for one hour with nitric oxide synthase inhibitors (L-NAME, SMT) or NO donors (SNP, DETA NONOate), a NO precursor (L-arginine), soluble guanylate cyclase inhibitors (ODQ, methylene blue), and a potassium channel blocker (TEA). Following 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 red blood cell deformability.




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