Central angiotensin induction of fetal brain c-fos expression and swallowing activity

Am J Physiol Regul Integr Comp Physiol. 2001 Jun;280(6):R1837-43. doi: 10.1152/ajpregu.2001.280.6.R1837.

Abstract

The present study examined physiological and cellular responses to central application of ANG II in ovine fetuses and determined the fetal central ANG-mediated dipsogenic sites in utero. Chronically prepared near-term ovine fetuses (130 +/- 2 days) received injection of ANG II (1.5 microg/kg icv). Fetuses were monitored for 3.5 h for swallowing activity, after which animals were killed and fetal brains were perfused for subsequent Fos staining. Intracerebroventricular ANG II significantly increased fetal swallowing in near-term ovine fetuses (1.1 +/- 0.2 to 4.5 +/- 1.0 swallows/min). The initiation of stimulated fetal swallowing activity was similar to the latency of thirst responses (drinking behavior) elicited by central ANG II in adult animals. ANG II evoked increased Fos staining in putative dipsogenic centers, including the subfornical organ, organum vasculosum of the lamina terminalis, and median preoptic nucleus. Intracerebroventricular injection of ANG II also caused c-fos expression in the fetal hindbrain. These results indicate that an ANG II-mediated central dipsogenic mechanism is intact before birth, acting at sites consistent with the dipsogenic neural network. Central ANG II mechanisms likely contribute to fetal body fluid and amniotic fluid regulation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Arteries / embryology
  • Brain / drug effects
  • Brain / embryology*
  • Cerebral Cortex / embryology
  • Deglutition / drug effects
  • Deglutition / physiology*
  • Electrocardiography
  • Fetus / metabolism
  • Fetus / physiology
  • Immunochemistry
  • Injections, Intraventricular
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Rhombencephalon / embryology
  • Sheep

Substances

  • Proto-Oncogene Proteins c-fos
  • Angiotensin II