Our purpose was to investigate the hemodynamic mechanism of flow recruitment within arteriolar networks as stimulated by the vitronectin receptor. Since remote stimulation of the vitronectin receptor initiates a flow-mediated dilation, we tested whether the response could be mimicked by exogenous NO. Arteriolar diameter, red blood cell flux, and velocity were measured in terminal branch arterioles arising from a central feed (8-10 microm) arteriole (together previously defined as an arteriolar network) in the cheek pouch tissue of anesthetized hamsters (n = 29, pentobarbital 70 mg/kg). Terminal branch arterioles were stimulated (micropipette, 10 s) with 10 microg/ml LM609 (agonist, vitronectin receptor), 10(-4) M nitroprusside (SNP), or control. The same amount of flow was recruited into the network by applying LM609 or SNP to only one branch of the network; however, flow distribution differed. With LM609, all recruited flow went directly to the branch that was stimulated. With SNP, recruited flow was distributed evenly throughout the network, no matter where the stimulus was applied. Thus, flow-mediated dilation induced by vitronectin receptor stimulation initiates a robust flow recruitment response, directing flow to the stimulus flow path. In contrast, NO alone initiates flow recruitment to the entire network, along multiple parallel flow paths.