Model of NO-induced inhibition of SSRBC adhesion. RBC NO or SNO may modulate (eg, inhibit) intercellular adhesion via autocrine mechanisms such as by binding to reactive cysteine residues in the relevant G protein–coupled receptors such as the beta₂-adrenergic receptor (β₂AR), its downstream signaling partners such as the S-type G-protein (G_αs), or an adhesion receptor such as LW/ICAM-4. Alternatively, SNO (but not NO) exported from RBCs may inhibit adhesion by acting on adjacent cells in paracrine fashion; for example, during RBC-endothelial cell (or RBC-leukocyte) contact, possibly functionally modifying a counterreceptor such as α-v-β-3 (α_vβ₃) integrin, or when transfused AARBCs mix with native, activated SSRBCs.