Nitric oxide (NO) interacts with hemoglobin (Hb) at its metal centers, whereas S-nitrosothiols (RSNOs) can donate the NO group to .beta.93 cysteine residues, thereby shielding the NO functionality from heme inactivation. S-nitrosylation of Hb is under the allosteric control of oxygen and the oxidation state of heme. NO group release from SNO-Hb is further facilitated by intracellular low molecular weight thiols, forming RSNOs which can be exported from the erythrocyte to regulate blood pressure. Red blood cells can be loaded with low molecular weight RSNOs to act as a delivery system for NO.sup.+ groups. Loaded red blood cells can be used in methods of therapy for conditions which are characterized by abnormal O.sub.2 metabolism of tissues, oxygen-related toxicity, abnormal vascular tone, abnormal red blood cell adhesion, or abnormal O.sub.2 delivery by red blood cells.
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