Hypertension, Vol 3, 313-317, Copyright © 1981 by American Heart Association
JE Szilagyi and CM Ferrario
Angiotensin II, when given into the vertebral arteries, acts at the area
postrema to augment central sympathetic vasomotor activity. The mechanism
of action is unknown but recent evidence implicates an interaction with the
opiate system. In dogs anesthetized with chloralose either alone or in
combination with morphine, naloxone blunted the pressor response to
vertebrally administered angiotensin II by 50%. Addition of morphine to
dogs anesthetized with chloralose only doubled the pressor response to
identical doses of angiotensin II. On the other hand, the magnitude of the
pressor responses to intravenously infused angiotensin II were unaltered by
either naloxone or morphine. Likewise, responses to norepinephrine given
vertebrally and intravenously were not similarly affected. Therefore,
naloxone-induced changes in vascular responsiveness were not responsible
for the altered sensitivity of the area postrema to angiotensin II
following blockade of endogenous opiates. The data suggest that there
exists a previously unrecognized interaction of the endogenous opiate
system in the medulla in mediating the pressor effects of angiotensin II at
the level of the area postrema.
ARTICLES
Central opiate system modulation of the area postrema pressor pathway
This article has been cited by other articles:
![]() |
H. P. DUSTAN Mechanisms of Hypertension Associated with Obesity Ann Intern Med, May 1, 1983; 98(5_Part_2): 860 - 864. [Abstract] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1981 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |