Background: Previous work has documented a 5-fold increase in Lp due to AngII. We hypothesized that the increase in Lp due to activation of the AT1 receptor is modulated by intracellular calcium [Ca2+]. Methods: Lp was measured in rat mesenteric venules using the Landis micro-occlusion model. A 100 mM KCl Ringer’s solution (HK) was used to abolish the electrochemical driving force for [Ca2+] influx. Measures of Lp were obtained at baseline (BL), after HK, and after 20 ng/ml AngII plus HK (n = 6). Modulation of [Ca2+] via selective AT1 activation was evaluated by: 1) measuring Lp at BL, after HK, and after 100 μM of the AT1 agonist Sar1-AngII in HK solution (n = 6), and 2) by measuring Lp after 25 μg/ml of the type 2 (AT2) receptor blocker PD-123319 (PD) in HK, and after PD plus AngII in HK (n = 6). Results: HK prevented the increase in Lp seen with AngII (Fig. 1). AT1 activation with both Sar1-AngII in HK (p = 0.001) (Fig 2) and AngII+PD in HK (p = 0.008) (Fig 3) slightly increased Lp, however, this effect was less than that observed with AT1 activation alone. Units for Lp are ×10–7 cm sec–1 · cm H2O–1. Conclusions: Inhibition of endothelial cell calcium influx prevented the 5-fold increase in Lp due to AngII alone and attenuated the 5-fold increase in Lp due to AT1 activation. This suggests that AngII activation of the AT1 receptor increases Lp primarily, but not exclusively, via modulation of intracellular calcium and raises the question of notable cross-talk between the AT1 and AT2 receptors.