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