Evidence that centrally released arginine vasopressin is involved
in central pressor action of angiotensin ii.
Slawomir, O., Ewa Szczepaska-Sadowska, and Maria Szczypaczewska.
Warsaw Medical Academy, Department of Clinical and Applied
Physiology, Warsaw, Poland
APStracts 2:0304H, 1995.
Five Series of experiments were performed on conscious trained dogs to
find out whether intracranially released arginine vasopressin (AVP)
is involved in mediation of central cardiovascular effects of
angiotensin II (ANGII). The dogs were implanted with guide tubes
leading to the third cerebral ventricle (ICV) and with the
intraarterial catheters. Blood pressure and heart rate were
continuously monitored during (ICV) administration of 1) ANGII alone
(250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANGII together
with AVP, 4) AVP together with AVP V1 receptors antagonist (MECAAVP,
V1ANT, 100 ng/min), and 5) ANGII together with V1ANT. The results
revealed that 1) ANGII and AVP applied separately elicited
significant, long-lasting increases of blood pressure, 2) The maximum
pressor effect after ANGII and AVP applied together did not differ
from that after separate application of either of these peptides but
the duration of the pressor response was significantly shorter, 3)
Pretreatment with V1ANT effectively prevented blood pressure
increases elicited by central administration of AVP and ANGII, 4)
After blockade of V1 receptors administration of AVP resulted in a
significant delayed decrease of blood pressure below baseline. The
results strongly suggest that 1) Centrally released AVP mediates the
the pressor effect of ICV applied ANGII by means of V1 receptors, 2)
ICV applied ANGII and AVP interact to activate the machanism involved
in extinction of their pressor effect, 3) Blockade of central V1
receptors uncovers the hypotensive action of centrally applied AVP
Received 9 January 1995; accepted in final form 11 July 1995.
APS Manuscript Number H16-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.