Hypertension, Vol 4, 827-838, Copyright © 1982 by American Heart Association
TJ Gregory, CJ Wallis and MP Printz
One approach to establish the existence and functionality of a brain
angiotensin system is to demonstrate selective alterations in that system
following perturbation of peripheral cardiovascular functions. The present
study utilized this approach to quantify regional angiotensinogen levels in
the rat brain following bilateral nephrectomy, a perturbation that severely
disrupts salt and water homeostasis. Angiotensinogen, the precursor of any
centrally-derived angiotensin, was analyzed since it should provide a
marker for a putative angiotensin peptidergic system. Net brain
angiotensinogen was determined by correcting total tissue concentrations of
angiotensinogen with accurate values of contaminating plasma
angiotensinogen. The latter was determined by quantifying regional plasma
space utilizing tritiated inulin as a marker of cerebral vascular space. It
was found that there were no detectable alterations in regional net brain
angiotensinogen in the first 24 hours following nephrectomy despite over a
twofold increase in plasma angiotensinogen and the absence of significant
plasma renin. By 32 hours postnephrectomy, certain areas of the rat
hypothalamus and midbrain exhibited significant elevations in net
angiotensinogen content. These areas coincided with regions traversed by
neural pathways shown to mediate angiotensin-induced drinking or blood
pressure elevations. The results lend further support to the concept of an
independent brain angiotensin system.
ARTICLES
Regional changes in rat brain angiotensinogen following bilateral nephrectomy
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1982 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |