Abstract only Multiple reports recognized that immunity participates in hypertension (HTN), although direct mechanisms that orchestrate the immune-vascular interaction are still unknown. Mice infused with AngiotensinII (AngII) typically increase blood pressure (BP), concomitantly recruiting immune cells in the vasculature, with CD8 T cells playing a crucial role. To investigate the molecular regulators of vascular-immune interface, we established a system of vessel organ culture, enabling the study of physiological properties of resistance arteries via a modified pressure myograph which keeps vessels alive and functional for several days, while co-culturing immune cells of interest. We tested potential direct effects of CD8 T cells isolated from AngII-HTN or vehicle mice on resistance arteries from naïve mice. After co-incubation in the organ culture, CD8 T cells from HTN mice significantly increased myogenic tone (MT) of arteries, while no effect was induced by CD8 T of vehicle mice (%MT=CD8 AngII :27±2; CD8 veh :16±2, p<0.01). Our previous studies showed that an intracellular signaling involved in the acquisition of CD8 effectors functions, phosphatidylinositol-3-kinase-γ (PI3Kγ), was also involved in AngII-induced HTN, being its inhibition protective toward increase in BP and in vascular resistance. Here we took advantage of a mouse model expressing constitutively active PI3Kγ (PI3Kγ CX ), to test immune functions of PI3Kγ in HTN. PI3Kγ CX showed a spontaneous hypertensive phenotype (SBP mmHg :129±1 vs WT:104±2, p<0.001) accompanied by infiltration of activated CD8 T cells in renal vasculature. Then, CD8 T cells isolated from PI3Kγ CX mice and placed in co-culture with WT arteries increased their MT. Conversely, the CD8 T cells from WT mice had no effect when cultured with vessels (%MT=CD8 CX :31±1; CD8 WT :19±1, p<0.001). To test the in vivo relevance, we performed an adoptive transfer of CD8 CX in WT mice, finding that they developed spontaneous HTN, while no effect was induced by CD8 WT (SBP mmHg : CD8 CX 128±2 vs CD8 WT 103±2, p<0.001). Taken together these data show that CD8 T cells from AngII-HTN mice are able to directly increase MT of resistance arteries and that PI3Kγ signaling is a crucial modulator of this effector function, likely contributing to BP increase.