Fig. 4.

Schematic summarizing the main findings of the study. Persistent (and unrestricted) insulin signaling does not alter vasomotor function in response to insulin (left); however, persistent insulin signaling in the setting where phosphatidylinositol-3 kinase (PI3K)/Akt signaling is depressed causes insulin-induced vasoconstriction (middle), thus recapitulating the pathophysiological phenomenon. This insulin-induced vasoconstriction is abolished with concurrent MAPK inhibition or endothelin-1 (ET-1) receptor antagonism (right). IR, insulin receptor.