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Abstract
We sought to determine whether arginine vasopressin (AVP) modulates arterial pressure
(AP) by a receptor-mediated action in the nucleus reticularis rostroventrolateralis
(nRVL). Immunocytochemical labeling with an antiserum against a synthetic AVP conjugate
revealed a discrete although modest presumptive neuropeptidergic innervation of the
nRVL. Electron microscopic analysis of vasopressinergic processes in the nRVL revealed
that AVP-like immunoreactivity (AVP-LI) was primarily in axons and axon terminals.
Immunoreactive terminals contained numerous small clear vesicles and large dense core
vesicles and formed synapses with unlabeled dendrites. In the nRVL, retrograde transport-immunofluorescence
data demonstrated close appositions between vasopressinergic beaded processes and
a compact subambigual column of reticulospinal neurons labeled by deposits of cholera
toxin beta-subunit into the thoracic spinal cord. Similar methods were used to define
the origins of the AVP-afferent projection to nRVL. These retrograde transport-immunofluorescence
studies demonstrated numerous retrogradely labeled neurons in the hypothalamus, including
the paraventricular nucleus (PVN), after injections of a retrograde tracer, Fluoro-Gold
into the ventrolateral medulla. However, double-labeled neurons were rare and confirmed
a diffuse AVP afferent innervation of the sympathoexcitatory area. Microinjection
of AVP into the nRVL in anesthetized rats produced a large dose-related increase in
AP different from control at a dose of 1 pmol or higher. AVP injected intravenously
elevated AP only at significantly higher doses. Microinjections of AVP into the nucleus
tractus solitarii (NTS) had a smaller effect whereas into the caudal ventrolateral
medulla exerted no effect on AP. Bilateral microinjections of an AVP antagonist, d(CH2)5[Tyr(Me)2]AVP
into the nRVL produced no change in AP but blocked the increase produced by subsequent
injections of AVP. An acute hemorrhage produced by withdrawal of 2 ml of blood from
the femoral vein did not alter AP. However, bilateral microinjections of the AVP antagonist
into the nRVL 5 min after hemorrhage decreased AP. In contrast, the AVP-antagonist
injected intravenously after hemorrhage had no effect on AP. Our data suggest that
under conditions demanding increased sympathetic drive to maintain AP, such as hemorrhage,
a functional AVP receptor mechanism via terminals in the nRVL may be activated to
restore normal levels of AP.