“…Endothelium‐derived nitric oxide (NO) is a potent vasodilatory gasotransmitter and its production and bioavailability has been found to be an important contributor to NVC responses (Toth et al., 2015). In aging, highly reactive excess superoxide (O 2 .− ) molecules sequester free NO to form peroxynitrate (ONOO ‐ ) thus decreasing bioavailability of endothelium‐derived NO, impairing the dilatory capability of the cerebromicrovasculature (Csiszar et al., 2002; Park et al., 2007; Tarantini et al., 2016; Tarantini et al., 2017; Tarantini et al., 2018). In support of the role of endothelial dysfunction in impaired NVC responses, experimental evidence suggests that treatments that restore endothelial function (Tarantini et al., 2018; Tarantini et al., 2019), improve NO bioavailability (Wiedenhoeft et al., 2019), inhibit NADPH oxidases (Park et al., 2007), or reduce cerebrovascular oxidative stress (Kiss et al., 2019; Tarantini et al., 2019; Toth et al., 2014) can improve NVC responses in aged animals.…”