This in vitro rat tail artery model demonstrates that cold-induced vasoconstriction is driven by augmented smooth muscle responsiveness to norepinephrine, while vasodilatation results from cessation of adrenergic transmitter release.
No takes yet. Share an insight, caveat, or question.
Caution against clinical extrapolation from rat arteries; leaves open adrenergic targets in human cold vasomotor disorders.
Gardner et al. (1986) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: