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01; Table 1 and Fig. 3B). In both Supine and HUT conditions, thigh-cuff release elicited a decrease in blood pressure (Fig. 4A). Changes in MAP from baseline to nadir in HUT were larger than those in Supine (P selleck chemical and VA trials (Table 2). The degree of the decrease in ICA blood flow and VA blood flow responses to cuff release was not different during Supine, while during HUT changes in VA blood flow to thigh-cuff release were larger than those in ICA blood flow (VA ?32.2 �� 1.7 versus ICA ?26.1 �� 1.8%; P and Fig. 5B). In contrast, dynamic CA in the ICA was not significantly attenuated during HUT (Supine 0.23 �� 0.02 versus HUT 0.20 �� 0.03 s?1; Table 2 and Fig. 5A). The major novel findings of the present investigation are that there is a differential blood flow response in the ICA and VA in response to orthostatic stress. While GPX4 blood flow in the ICA and MCA Vmean were reduced during HUT, VA blood flow was well maintained. This preservation of VA blood flow may be a beneficial response for regulating the systemic circulation during orthostatic stress. Moreover, the attenuation in RoR during HUT in the VA suggests that there may be differences in dynamic CA between two major brain vascular areas in response to an acute change in perfusion pressure during orthostatic stress. Deegan et al. (2010) attempted to demonstrate the responses of CBF for the different vessels to orthostatic stress in healthy adults. They reported that the decline in blood flow velocity during orthostatic stress was similar in the MCA and VA. Moreover, they did not find any differences in dynamic CA between MCA and VA. This discrepancy may relate to differences in the period of examination and/or the degree of the orthostatic stress, because Deegan et al. (2010) used severe orthostatic stress, which combined HUT at 70 deg with lower body negative pressure to presyncope. Furthermore, in the present study, we evaluated the blood flow extracranially, using the portion of the VA in the cervical region, while Deegan et al. (2010) used TCD measurements to assess intracranial Osimertinib mw blood flow velocity (from the transforaminal window) in the VA. Given the possibility for differences in regulatory mechanisms controlling intracranial and extracranial blood flow, this may also contribute to inconsistencies between the present study and the work of Deegan et al. (2010). Importantly, Deegan et al. (2010) identified only CBF velocity during HUT, rather than CBF, because of the limitation of TCD measurement. Indeed, the TCD measurement is useful for identifing changes in CBF only when the arterial diameter is unchanged.