Hypoxia-induced cutaneous vasodilatation blunts cold-induced vasoconstriction via nitric oxide synthase-dependent mechanisms.
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No immediate clinical implications for cold-hypoxia interactions; extends mechanistic understanding of cutaneous vasomotor control.
When separated from local cooling, whole body cooling elicited cutaneous reflex vasoconstriction via mechanisms independent of nitric oxide removal. Hypoxia elicited cutaneous vasodilatation via mechanisms mediated primarily by nitric oxide synthase, rather than xanthine oxidase-mediated nitrite reduction. Cold-induced vasoconstriction was blunted by the opposing effect of hypoxic vasodilatation, whereas the underpinning mechanisms did not interrelate in the absence of local cooling. Full vasoconstriction was restored with nitric oxide synthase inhibition.
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Arnold et al. (2020) studied this question.
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