Sex differences in the vascular response to sympathetic activation during acute hypoxemia

Activation of the sympathetic nervous system causes vasoconstriction and a reduction in peripheral blood flow. Sympathetically-mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically-mediated vasocon...

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Veröffentlicht in:Experimental physiology 2021-07, Vol.106 (8), p.1689-1698
Hauptverfasser: Jacob, Dain W., Harper, Jennifer L., Ivie, Clayton L., Ott, Elizabeth P., Limberg, Jacqueline K.
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container_issue 8
container_start_page 1689
container_title Experimental physiology
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creator Jacob, Dain W.
Harper, Jennifer L.
Ivie, Clayton L.
Ott, Elizabeth P.
Limberg, Jacqueline K.
description Activation of the sympathetic nervous system causes vasoconstriction and a reduction in peripheral blood flow. Sympathetically-mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically-mediated vasoconstriction is preserved or even enhanced during hypoxemia. Given the potential for sex-specific differences in hypoxic vascular control, prior results are limited in application. We tested the hypothesis that young women attenuate sympathetically-mediated vasoconstriction during steady-state hypoxemia, whereas men do not. Healthy young men (n=13, 25±4 yrs) and women (n=11, 24±4 yrs) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxemia. Beat-to-beat blood pressure (BP, finger photoplethysmography) and forearm blood flow (FBF, venous occlusion plethysmography) were measured continuously. Total and forearm vascular conductance (TVC and FVC, respectfully) were calculated. A change (Δ) in TVC and FVC from steady-state during the last 1-min of CPT was calculated and differences between normoxia and systemic hypoxia were assessed. In men, the reduction in TVC during CPT was greater during hypoxia compared to normoxia (ΔTVC, p=0.02), whereas ΔTVC did not differ between conditions in women (p=0.49). In men, ΔFVC did not differ between normoxia and hypoxia (p=0.92). In women, the reduction in FVC during CPT was attenuated during hypoxia (ΔFVC, p
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Sympathetically-mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically-mediated vasoconstriction is preserved or even enhanced during hypoxemia. Given the potential for sex-specific differences in hypoxic vascular control, prior results are limited in application. We tested the hypothesis that young women attenuate sympathetically-mediated vasoconstriction during steady-state hypoxemia, whereas men do not. Healthy young men (n=13, 25±4 yrs) and women (n=11, 24±4 yrs) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxemia. Beat-to-beat blood pressure (BP, finger photoplethysmography) and forearm blood flow (FBF, venous occlusion plethysmography) were measured continuously. Total and forearm vascular conductance (TVC and FVC, respectfully) were calculated. A change (Δ) in TVC and FVC from steady-state during the last 1-min of CPT was calculated and differences between normoxia and systemic hypoxia were assessed. In men, the reduction in TVC during CPT was greater during hypoxia compared to normoxia (ΔTVC, p=0.02), whereas ΔTVC did not differ between conditions in women (p=0.49). In men, ΔFVC did not differ between normoxia and hypoxia (p=0.92). In women, the reduction in FVC during CPT was attenuated during hypoxia (ΔFVC, p&lt;0.01). We confirm sympathetically-mediated vasoconstriction is preserved or enhanced during hypoxemia in young men, whereas peripheral vascular responsiveness to sympathetic activation during hypoxemia is attenuated in young women. 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title Sex differences in the vascular response to sympathetic activation during acute hypoxemia
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