Two main hypotheses describe the role of hemoglobin in the regulation of nitric oxide (NO) bioavailability. It has been suggested that hemoglobin interacts with circulating NO, forming Fe-nitrosyl hemoglobin and then S-nitrosothiols, which deliver NO extracellularly by an allosterically regulated mechanism. Alternatively, the existence of diffusional barriers that protect NO from hemoglobin-mediated degradation has been proposed. The reliability of each model in vivo is supported by the detection of physiological hematic levels of S-nitrosohemoglobin. However, the measured concentrations of S-nitrosohemoglobin are largely divergent between the two models. Moreover, recent reports suggest that circulating levels of S-nitrosohemoglobin in human blood could be significantly lower than assessed previously. We suggest that solving the methodological controversies that make the field of NO research a 'minefield', even for skilled analysts, is fundamental to understanding the role of S-nitrosothiols in the vasculature.
|Titolo:||Nitric oxide, S-nitrosothiols and hemoglobin: is methodology the key?|
ROSSI, RANIERI (Corresponding)
|Citazione:||Giustarini, D., Milzani, A., Colombo, R., DALLE DONNE, I., & Rossi, R. (2004). Nitric oxide, S-nitrosothiols and hemoglobin: is methodology the key?. TRENDS IN PHARMACOLOGICAL SCIENCES, 25(6), 311-316.|
|Appare nelle tipologie:||1.1 Articolo in rivista|