Fig. 9.

Schematic representation of the role of β integrins in mediating FAK Y397 autophosphorylation of the resistance arteries. a Normotenisve: integrin α5β1 (involved in calcium influx) and β3 integrin subunits are mechanically activated resulting in FAK Y397/Src Y418 phosphorylation, and are probably required for normal vascular integrity during normotensive pressure fluctuations. Relatively little change in FAK Y397 and Scr Y418 phosphorylation is required for normal vascular adaptations to minor changes in pressure. Signaling of FAK/Src via ‘general’ ECM-anchoring β1 integrins is minimal. b Hypertensive inward remodeling with cRADfV: during hypertensive remodeling, an increase in phosphorylation of the mechanosensitive FAK Y397/Src Y418 signaling complex is mediated via β1 and β3 integrins (but not the pSrc Y418 component of α5β1), suggesting a role of β1 and β3 integrin subunits to maintain vascular integrity in response to an increase in pressure. c Hypertrophic remodeling: abrogation of αVβ3 signaling with cRGDfV results in hypertrophy in response to pressure and mechanosignaling exclusively through β1 integrins. The majority of the β1 integrins are thought to be important in ‘anchoring’ VSMCs within the matrix of the vascular wall. Exclusive mechanosensing of FAK Y397 via β1 integrins through this rigid scaffold is thought to be central to these structural adaptations in hypertension.