Sex differences may play a significant role in determining the risk of hypertension. Bulbospinal neurons in the rostral ventrolateral medulla (RVLM) are involved in the tonic regulation of arterial pressure and participate in the central mechanisms of hypertension. Angiotensin II (AngII) acting on angiotensin type 1 (AT₁) receptors in RVLM neurons is implicated in the development of hypertension, by activating NADPH oxidase and producing reactive oxygen species (ROS). Therefore, we analyzed RVLM bulbospinal neurons to determine whether there are sex differences in: 1) immunolabeling for AT₁ receptors and the key NADPH oxidase subunit p47 using dual-label immunoelectron microscopy, and 2) the effects of AngII on ROS production and Ca²⁺ currents using, respectively, hydroethidine fluoromicrography and patch clamping. In tyrosine hydroxylase-positive RVLM neurons, female rats displayed significantly more AT₁ receptor immunoreactivity and less p47 immunoreactivity than male rats (p<0.05). Although AngII (100 nM) induced comparable ROS production in dissociated RVLM bulbospinal neurons of female and male rats (p>0.05), an effect mediated by AT₁ receptors and NADPH oxidase, it triggered significantly larger, dihydropyridine-sensitive long-lasting (L-type) Ca²⁺ currents in female RVLM neurons (p<0.05). These observations suggest that an increase in AT₁ receptors in female RVLM neurons is counterbalanced by a reduction in p47 levels, such that AngII-induced ROS production does not differ between females and males. Since the Ca²⁺ current activator BayK8644 induced larger Ca²⁺ currents in females than in male RVLM neurons, increased AngII-induced L-type Ca²⁺ currents in females may result from sex differences in calcium channel densities or dynamics.