Acute stress increases venomotor tone in conscious rats..
Martin, D. S., C. Appelt, M. C. Rodrigo, and M. E. Egland.
Department of Physiology and Pharmacology, University of South
Dakota, 414 East Clark Street, Vermillion SD 57069
APStracts 3:0054H, 1996.
This study tested the hypothesis that acute psychological stress
causes venoconstriction. Male Sprague Dawley rats were instrumented
with indwelling catheters in a femoral artery and vein and a balloon
tipped catheter in the right atrium. Arterial pressure, venous
pressure, heart rate, and mean circulatory filling pressure (MCFP)
were monitored in conscious rats. Air jet stress was performed before
and after treatment with saline, chlorisondamine, phentolamine or
prazosin. Air jet stress caused MAP, HR and MCFP to increase by 10
+/- 1 mmHg, 31 +/- 4 b.p.m., and 0.95 +/- 0.09 mmHg respectively.
Treatment with either chlorisondamine or phentolamine were equally
effective in abolishing the stress-induced increases in MAP, HR and
MCFP. Prazosin treatment abolished the pressor response to air jet
stress but did not significantly affect the HR and MCFP responses. In
contrast, pretreatment with the alpha 2 receptor antagonist
rauwolscine hydrochloride abolished both the MAP and MCFP responses
to air jet stress but did not affect the HR response. These findings
indicate that venoconstriction is an important component of the
cardiovascular response to acute psychological stress. Stress induced
venoconstriction appears to be mediated primarily via the alpha2
receptor subtype.
Received 14 November 1994; accepted in final form 24 January
1996.
APS Manuscript Number H1017-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96