Sex differences in the vascular response to sympathetic activation during acute hypoxaemia, 2021, Jacob et al

SNT Gatchaman

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Sex differences in the vascular response to sympathetic activation during acute hypoxaemia
Jacob DW, Harper JL, Ivie CL, Ott EP, Limberg JK

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 hypoxaemia. 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 hypoxaemia, whereas men do not. Healthy young men (n = 13, 25 ± 4 years) and women (n = 11, 24 ± 4 years) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxaemia. Beat-to-beat blood pressure (finger photoplethysmography) and forearm blood flow (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 < 0.01). We confirm sympathetically mediated vasoconstriction is preserved or enhanced during hypoxaemia in young men, whereas peripheral vascular responsiveness to sympathetic activation during hypoxaemia is attenuated in young women. The results advance our understanding of sex-related differences in hypoxic vascular control.

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Posting in relation to potential pathomechanisms in POTS being female-predominant.

Main conclusions from the present study are three-fold:
1) sympathetically-mediated vasoconstriction does not differ between men and women during normoxia
2) the systemic vasoconstrictor response to sympathetic activation is augmented during hypoxemia in men, but not in women
3) the local forearm vasoconstrictor response to sympathetic activation is attenuated during hypoxemia in women only

Under normoxic conditions, sympathetic activation results in stimulation of α-adrenergic receptors on vascular smooth muscle and downstream vasoconstriction.

Estrogen also increases production of nitric oxide (Sudhir et al., 1996), which is important contributor to compensatory hypoxic vasodilation

Our results demonstrate hypoxia differentially modulates vascular responsiveness to sympathetic activation in men and women. Present data support previous findings that sympathetically-mediated vasoconstriction is preserved or enhanced in men during systemic hypoxia, and provide new data to show sympathetically-mediated vasoconstriction is attenuated during hypoxemia in young women.
 
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