The role of parabrachial nucleus in baroreflex mediated coronary
vasoconstriction.
Gutterman, David D., Angie Goodson.
VA Medical Center and Department of Internal Medicine, University
of Iowa, Iowa City, Iowa
APStracts 3:0102H, 1996.
Coronary vasoconstriction is a component of the baroreflex response to
bilateral carotid occlusion. The central pathways responsible for
this reflex constriction are incompletely understood but previous
studies show that activation of parabrachial nucleus elicits coronary
vasoconstriction and that parabrachial nucleus shares prominent
anatomic connections with other central baroreflex centers including
the nucleus of the tractus solitarius. Therefore we examined whether
PBN plays a role in baroreflex mediated coronary constriction and
whether cell bodies rather than fibers passing through this region
are involved. Anesthetized cats were instrumented for continuous
measurements of heart rate, arterial pressure and coronary flow
velocity. Bilateral carotid occlusion following propranolol and
vagotomy increased arterial pressure (63+10%) and an index of
coronary vascular resistance (34+6%). Bilateral microinjections of
lidocaine (1%, 400 nl) into PBN reversibly attenuated the coronary
constriction (19+5%) with little effect on the change in arterial
pressure. It was further demonstrated that autoregulatory responses
to the increase in pressure could not fully account for the observed
changes in coronary constriction. In a separate group of animals
kainic acid (50 mM, 300 nl) abolished the baroreflex increase in
coronary resistance (43+1 vs -9+9% after) without affecting the
increase in arterial pressure (54+12% increase before vs 55+20%
increase after KA). We conclude that parabrachial nucleus is a
necessary component of the baroreflex pathway mediating coronary
vasoconstriction. Furthermore cell bodies in parabrachial nucleus
rather than simply fibers passing through that region participate in
the reflex coronary vasoconstriction.
Received 30 May 1995; accepted in final form 5 January 1996.
APS Manuscript Number H493-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96