Subcellular mechanisms of angiotensin ii (ang ii) and arginine
-vasopressin (avp) activation of area postrema neurons.
Consolim-Colombo, Fernanda M., Meredith Hay, Thomas C. Smith, and
Vernon S. Bishop.
Department of Physiology, The University of Texas Health Science
Center at San Antonio, San Antonio, Texas, Department of
Hypertension, University of Sao Paulo/Heart Institute, Sao Paulo,
Brazil
APStracts 3:0083R, 1996.
Angiotensin II (ANG II) and arginine vasopressin (AVP) act on area
postrema (AP) neurons to modulate the baroreflex. Since activation of
AP neurons by either ANG II or AVP increases intracellular free
calcium concentrations ([Ca++]i), the goal of this study was to
analyze the factors affecting the [Ca++]i responses to ANG II and
AVP. Neurons were recovered from 14 - 16 day old rats and studied
after 8 - 14 days in culture using the microscopic digital image
analysis for Fura-2 loaded cells. The effects of ANG II (100 nM) and
AVP (100 nM) on [Ca++]i were determined in normal (2 mM) and low
(&LT10 nM) extracellular calcium concentrations. In 143 out of 240
neurons, ANG II increased [Ca++]i 4.65 X after 20 sec, and a similar
response was observed in the absence of extracellular calcium (3.65 X
after 20 s). After 60 sec of observation, steady-state levels of
increased [Ca++]i were still present under both conditions.
Pretreatment with AT1 antagonist or pertussis toxin abolished the
response to ANG II. AVP also increased [Ca++]i (3.6 X -peak 20 s) in
normal and low extracellular calcium. Pretreatment with AVP1
antagonist or pertussis toxin abolished the response to AVP. This
study indicates that ANG II-induced increases in [Ca++]i are
independent of extracellular calcium concentrations, and involve the
activation of AT1 receptors and a pertussis toxin sensitive G
protein. While AVP affects a fewer number of AP neurons, the
mechanisms of activation are also independent of extracellular
calcium concentration, and are mediated by a pertussis toxin
sensitive G protein.
Received 31 July 1995; accepted in final form 12 January 1996.
APS Manuscript Number R477-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96