Effect of vasopressin on baroreflex control of lumbar sympathetic
nerve activity and hindquarter resistance.
Scheuer, Deborah A., and Vernon S. Bishop.
Departments of Pharmacology and Physiology, The University of Texas
Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas
78284
APStracts 2:0499H, 1995.
Arginine vasopressin (AVP) has been shown to increase the inhibitory
influence of the baroreflex on sympathetic nerve activity by a
mechanism involving receptors located in the area postrema. The
purpose of these experiments was to study the functional effect of
this action of AVP by testing the hypothesis that AVP can buffer its
own vasoconstrictor effect by facilitating baroreflex-mediated
withdrawal of sympathetic nerve activity. Specifically, we determined
1) if arginine vasopressin (AVP) can attenuate increases in
hindquarter vascular resistance during the infusion of another
vasoconstrictor, phenylephrine and 2) whether the effects of AVP on
vascular resistance are associated with appropriate corresponding
changes in lumbarsympathetic nerve activity. In pentobarbital
-anesthetized New Zealand White rabbits the baroreflex was stimulated
by phenylephrine-induced elevations in arterial pressure. Baroreflex
-mediated changes in heart rate (HR), calculated hindquarter vascular
resistance index (R) and lumbar sympathetic nerve activity (LSNA)
were determined during the simultaneous intravertebral infusion of
AVP (0, 0.5 or 1.0 ng/kg/min). Intravertebral infusion of AVP alone
had no effect on resting MAP, but reduced baseline values for LSNA
and HR. Intravenous infusion of phenylephrine alone produced dose
-dependent increases in MAP and R and decreases in LSNA and HR. The
simultaneous infusion of AVP (0.5 or 1.0 ng/kg/min) and phenylephrine
(1.25, 2.5, 5.0, 7.5 and 10.0 [mu]g/kg/min) had no effect on the
increase in MAP, but attenuated the increases in R and facilitated
the reductions in LSNA at all doses of phenylephrine. The higher dose
of AVP also enhanced the phenylephrine-induced reductions in HR. In
contrast, the intravenous infusion of AVP (1.0 ng/kg/min) did not
alter baroreflex mediated changes in R, LSNA or HR. Therefore, we
conclude that the action of AVP to increase baroreflex mediated
sympathoinhibition results in an attenuated rise in hindquarter
vascular resistance during the infusion of another vasoconstrictor,
phenylephrine.
Received 8 March 1995; accepted in final form 25 October 1995.
APS Manuscript Number H222-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95