Brain C-FOS expression and pressor responses after I.V. or I.C.V. angiotensin in the near-term ovine fetus.

Fetal brain c-fos and cardiovascular responses after i.v. or i.c.v. angiotensin II administrations was determined in the near-term ovine fetuses. Both routes of angiotensin II markedly increased fetal mean arterial pressure. The latency of pressor responses by i.v. angiotensin II administration was shorter than by the i.c.v. route. The increased fetal mean arterial pressure was greater and transient by the i.v. route in comparison to that caused by i.c.v. angiotensin II administration. Following the i.v. administration of angiotensin II, the fetal heart rate was significantly decreased. Associated with fetal pressor responses and bradycardia, c-fos expression induced by i.v. angiotensin II was in the paraventricular nuclei (PVN) of the hypothalamus, and the area postrema, the tractus solitarius nuclei, and the lateral parabrachial nuclei in the brain stem. After i.c.v. angiotensin II administration, fetal blood pressure was also increased in association with the intensive c-fos expression in the PVN and the hindbrain. However, fetal heart rate was not affected by the central injection of angiotensin II. These results indicate that the central pathways between the forebrain circumventricular organs and the PVN have developed, and suggest that the neural activity in the hindbrain associated with bradycardia may be linked to the baroreflex. In the face of i.c.v. angiotensin II, sympathetic activation may play a predominant role in pressor responses. Taken together, these results suggest that central and peripheral angiotensin II-induced fetal pressor responses may be mediated by separate mechanisms, and these regulatory mechanisms start to function by near-term or early.