Table 2

Vasoactive effect of adipokinesa


Vasoactive effect


Superoxide anion

Vasoconstriction through Ca2+ sensitization; impairs EC-dependent relaxation by decreasing NO bioavailability; enhances vasoconstriction to perivascular nerve activation by electrical field stimulation


Hydrogen peroxide

EC-dependent and EC-independent vasorelaxation mediated by opening KCa, Kv and KATP channels; Ca2+-dependent and Ca2+-independent vasoconstriction



Vasoconstriction due to sympathetic nervous system activation; EC-dependent and EC-independent vasorelaxation



EC-dependent and EC-independent vasorelaxation; triggers ET-1- and Ang-induced vasoconstriction; impairs EC-dependent vasorelaxation due to decreased NO or increased ROS production; reduces vasorelaxing effect of PVAT due to increased ROS production



EC-independent vasorelaxation; reduces vasorelaxing effect of PVAT due to increased ROS production; impairs endothelial function due to increased ROS and decreased NO production



NO-dependent vasorelaxation; EC-independent vasoconstriction



NO-dependent vasorelaxation mediated by opening Kv channels



EC-dependent and EC-independent vasorelaxation



NO-dependent vasorelaxation



Vasorelaxation through opening of KATP, KCNQ or KCa channels depending on the species


Ang II

Vasoconstriction via binding on AT1 receptors



No effect on contractility of blood vessels; impairs endothelial function due to increased ET-1 production and decreased NO production


aEC, endothelial cell; NO, nitric oxide; KCa channels, Ca2+-activated K+ channels; Kv channels, voltage-dependent K+ channels; KATP channels, ATP-sensitive K+ channels; TNFα, tumor necrosis factor α; ET-1, endothelin 1; Ang, angiotensinogen; ROS, reactive oxygen species; PVAT, perivascular adipose tissue; IL-6, interleukin 6; Ang II, angiotensin II; AT1, angiotensin type 1; ADRF, adipocyte-derived relaxing factor.

Maenhaut and Van de Voorde BMC Medicine 2011 9:25   doi:10.1186/1741-7015-9-25

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