Pregnancy is characterized by increased blood volume and baseline sympathetic nerve activity (SNA), vasodilation, and tachycardia. Relaxin (RLX), an ovarian hormone elevated in pregnancy, activates forebrain sites involved in control of blood volume and SNA through angiotensin (Ang II) dependent mechanisms, and contributes to adaptations during pregnancy. In anesthetized arterial baroreceptor denervated nonpregnant (NP) rats, RLX microinjected into the subfornical organ (SFO, 0.77 pmol in 50 nl) produced sustained increases in lumbar SNA (8 ± 3%) and mean arterial pressure (MAP, 26 ± 4 mmHg). Low dose intra-carotid artery (ica) infusion of RLX (155 pmol/ml/hr; 1.5 hr) had minor transient effects on arterial pressure and activated neurons (increased Fos-IR) in the SFO and in spinally-projecting (19 ± 2%) and AVP-IR (21 ± 5%) cells in the paraventricular nucleus of the hypothalamus (PVN) of NP, but not pregnant (P) rats. However, mRNA for RLX and Ang II AT1a receptors in the SFO were preserved in pregnancy. RLX receptor-IR is present in the region of the SFO in NP and P rats and is localized in astrocytes, the major source of angiotensinogen in the SFO. These data provide an anatomical substrate for a role of RLX in resetting of AVP secretion and increased baseline SNA in pregnancy. Since RLX and Ang II receptor expression was preserved in the SFO of P rats, we speculate that the lack of response to exogenous RLX may be due to maximal activation by elevated endogenous levels of RLX in near-term pregnancy.