Nitroprusside inhibits calcium-induced impairment of red blood cell deformability

Background Red blood cell (RBC) deformation is critical for microvascular perfusion and oxygen delivery to tissues. Abnormalities in RBC deformability have been observed in aging, sickle cell disease, diabetes, and preeclampsia. Although nitric oxide (NO) prevents decreases in RBC deformability, the underlying mechanism is unknown. Study Design and Methods As an experimental model, we used ionophore A23187–mediated calcium influx in RBCs to reduce their deformability and investigated the role of NO donor sodium nitroprusside (SNP) and KCa3.1 (Gardos) channel blockers on RBC deformability (measured as elongation index [EI] by microfluidic ektacytometry). RBC intracellular Ca2+ and extracellular K+ were measured by inductively coupled plasma mass spectrometry and potassium ion selective electrode, respectively. Results SNP treatment of RBCs blocked the Ca2+ (approx. 10 μmol/L)‐induced decrease in RBC deformability (EI 0.34 ± 0.02 vs. 0.09 ± 0.01, control vs. Ca2+ loaded, p