Central renin-angiotensin system is important in the control of blood pressure in the adult. However, few data exist about the in utero development of central angiotensin-mediated pressor responses. Our recent studies have shown that application of angiotensin II into the fetal brain can increase blood pressure at nearterm. The present study determined fetal blood pressure and heart rate in response to central application of angiotensin II in the chronically prepared preterm ovine fetus, determined the action sites marked by c-fos expression in the fetal central pathways following intracerebroventricular injection of angiotensin II in utero, and determined angiotensin subtype 1 receptors in the fetal hypothalamus. Central injection of angiotensin II significantly increased fetal mean arterial pressure (MAP). Adjusted fetal MAP against amniotic pressure was also increased by angiotensin II. Fetal heart rate was subsequently decreased following the central administration of angiotensin II and / or the increase of blood pressure. Angiotensin II induced c-fos expression in the central putative cardiovascular area - the paraventricular nuclei in the brain sympathetic pathway. Application of angiotensin II also caused intense FOSimmunoreactivity in the tractus solitarius nuclei in the hindbrain. In addition, intense angiotensin subtype 1 receptors were expressed in the hypothalamus at preterm. These data demonstrate that central angiotensin II-related pressor centers start to function as early as at preterm and suggest that the central angiotensin-related sympathetic pathway is likely intact in the control of blood pressure in utero.