Actions of angiotensin in the subfornical organ and area postrema: implications for long term control of autonomic output

Clin Exp Pharmacol Physiol. 1997 Jan;24(1):96-101. doi: 10.1111/j.1440-1681.1997.tb01790.x.

Abstract

1. Considerable physiological and anatomical evidence indicates that circulating angiotensin II (AngII), plays important roles in the long-term regulation of autonomic output as a result of actions in two circumventricular structures, the subfornical organ (SFO) and area postrema (AP). 2. Extracellular recordings have demonstrated excitatory actions of AngII on neurons from both of these structures which are AT1 receptor mediated, maintained when cells are placed in synaptic isolation, and are dose dependent. Interestingly SFO neurons appear to be an order of magnitude more sensitive to AngII than those in AP. 3. Recent calcium imaging studies have demonstrated that AngII induces increases in intracellular calcium in both SFO and AP neurons. Whole cell patch recordings have also begun to provide important information suggesting that AngII actions may modulate voltage activated ion channels in these two structures to elicit its observed actions on circumventricular organs (CVO) neurons at the blood-brain interface. 4. Through these actions circulating AngII is thus able to influence efferent projections from these CVO which in turn influence the output of hypothalamic cells projecting to the posterior pituitary (vasopressin secretion), nucleus tractus solitarius (NTS), and intermediolateral cell column of the spinal cord (to influence sympathetic preganglionics), and medullary neurons in the NTS.

Publication types

  • Congress
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin II / metabolism
  • Angiotensin II / physiology*
  • Animals
  • Autonomic Nervous System / physiology*
  • Cerebral Ventricles / physiology*
  • Feedback / physiology
  • Paraventricular Hypothalamic Nucleus / physiology
  • Subfornical Organ / physiology*
  • Time Factors

Substances

  • Angiotensin II