Table 2 Vasoactive effect of adipokines^a

Superoxide anion

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

[18, 19, 29]

Hydrogen peroxide

EC-dependent and EC-independent vasorelaxation mediated by opening K_Ca, K_v and K_ATP channels; Ca²⁺-dependent and Ca²⁺-independent vasoconstriction

[20, 21, 23–27]

Leptin

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

[31–34, 38, 39]

TNFα

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

[50, 52, 53, 57–59]

IL-6

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

[59, 66, 67, 72]

Apelin

NO-dependent vasorelaxation; EC-independent vasoconstriction

[76–78, 80]

Adiponectin

NO-dependent vasorelaxation mediated by opening K_v channels

[59, 90, 91]

Omentin

EC-dependent and EC-independent vasorelaxation

[100]

Visfatin

NO-dependent vasorelaxation

[107]

ADRF

Vasorelaxation through opening of K_ATP, KCNQ or K_Ca channels depending on the species

[6, 92, 112, 114, 115]

Ang II

Vasoconstriction via binding on AT1 receptors

[124]

Resistin

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

[135, 144]