It is generally believed that the erythrocyte membrane is highly permeable
to nitric oxide (NO). To prevent NO from freely entering and being scavenge
d by the red blood cell (RBC), it has been suggested that NO consumption is
limited by the mass transfer resistance of the diffusion layer adjacent to
the erythrocyte membrane. Recently, we (Vaughn et al. (2000). J. Biol. Che
m. 275, 2342) presented an experimental technique that overcomes experiment
al diffusional limitations and showed that RBCs also possess a mechanism to
slow nitric oxide uptake. Here, we present a mathematical analysis of this
technique by modeling the NO uptake of a single cell. We obtain additional
data (n = 33, total) by use of the competition experiment and, through app
lication of the model, show that either the RBC membrane permeability to NO
or the intracellular reaction rate between NO and hemoglobin (Hb) is at le
ast 2000-fold lower than previously thought. As a result, RBCs react with N
O at a rate three orders of magnitude slower than free oxyHb. This phenomen
a may play an important role in NO bioitvailability. (C) 2001 Academic Pres
s.