Rat vasopressin cell responses to simulated hemorrhage: stimulus
-dependent role for a1 noradrenaline neurons.
Smith, D. W., J. R. Sibbald, S. Khanna, and T. A. Day.
Department of Physiology and Pharmacology, University of
Queensland, Queensland 4072, Australia
APStracts 2:0061R, 1995.
c-Fos expression mapping and electrophysiological recording
experiments were done to clarify the role of the A1 noradrenergic
cell group in the vasopressin response to hypotensive hemorrhage. In
pentobarbital-anesthetized rats moderate and severe hypotensive
hemorrhages were simulated by brief occlusion of the inferior vena
cava sufficient to reduce mean arterial pressure to approximately 50
mmHg or 30 mmHg, respectively. Both stimuli significantly increased
the number of A1 region catecholamine cells displaying Fos-like
immunoreactivity, this effect being most prominent at the level of
the area postrema. Both stimuli also increased the number of
supraoptic nucleus vasopressin cells displaying Fos-like
immunoreactivity. Accordingly, electrophysiological studies involving
separate animals confirmed that both moderate and severe caval
occlusion significantly increased the firing of functionally
identified vasopressin cells recorded in the supraoptic nucleus.
However, while interruption of A1 region neuronal function by
injection of g-aminobutyric acid at the level of the area postrema
eliminated the increase in vasopressin cell firing elicited by
moderate caval occlusion, it did not block the response to severe
caval occlusion. These findings suggest that, in the rat, the
vasopressin response to an acute reduction in central blood volume,
such as that produced by hemorrhage, depends upon the A1 projection
only if the stimulus is of moderate intensity. Severe stimuli appear
to involve activation of both the A1 projection and an additional
vasopressin-stimulatory pathway which bypasses the A1 region.
Received 25 October 1994; accepted in final form 16 February
1995.
APS Manuscript Number R617-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 7 March 1995.