Acute exposure to
hypoxia evokes changes in local
vasodilator and neural
vasoconstrictor factors that significantly influence vascular tone. In humans, the net effect of acute systemic
hypoxia is limb vasodilation despite significant reflex increases in muscle sympathetic
vasoconstrictor nerve activity and
norepinephrine spillover. In this context, some studies in experimental animals and humans have documented that
hypoxia can reduce the
vasoconstrictor responses to sympathetic nerve stimulation, as well as exogenous
alpha-adrenergic agonist administration (functional sympatholysis). In contrast, other studies have provided evidence that sympathetic vasoconstriction is well preserved during
hypoxia. Recently, our laboratory demonstrated that local blockade of
alpha-adrenergic receptors significantly augments the forearm
vasodilator response to
hypoxia, indicating that sympathetic vasoconstriction persists and can restrain skeletal muscle blood flow under these conditions. Therefore, we revisited this issue and performed a study designed to test the hypothesis that forearm
vasoconstrictor responses to local endogenous
norepinephrine release are not reduced during systemic
hypoxia in humans. To do so, we used selective
intra-arterial infusions tyramine to evoke local endogenous
norepinephrine release and measured the forearm
vasoconstrictor responses during various levels of
hypoxia (85, 80, and 75 % O2 saturation). Our findings demonstrate that forearm post-junctional alpha-
adrenergic vasoconstrictor responsiveness is well preserved during systemic
hypoxia in healthy humans. The implications of these findings with respect to arterial blood pressure regulation and functional sympatholysis in skeletal muscle are discussed.