Reply to "SNO-hemoglobin and hypoxic vasodilation"

Rakesh Patel¹ & Tim Townes²

In response to our recent paper¹, Stamler et al. state that "an extensive body of evidence from our own and other laboratories supports a major role for SNO-Hb [S-nitrosohemoglobin] (in which a nitric oxide (NO) group is covalently coupled to Cys93 within the -chain [Cys93]) in the physiological response of hypoxic vasodilation..." However, we demonstrated that mutation of Cys93 to alanine has a surprisingly minor phenotype in our humanized mouse model. We state in our paper, "Cys93 is not essential for normal development or physiology under basal or exercise-stress conditions, that the absence of SNO-Hb does not result in pulmonary hypertension under normal conditions and that SNO-Hb is not required for RBCs to stimulate hypoxic vasodilation ex vivo.

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