Atrial natriuretic peptide in multiple system atrophy.
Bevilacqua, Maurizio, Guido Norbiato, Velella Righini, Lucia Castelli,
Angela Rogolino, Raffaello Furlan, Simona Piazza, Enrica Chebat, and
Tarcisio Vago.
Servizio di Endocrinologia, Divisione di Medicina II, Ospedale L.
Sacco (Vialba), Via GB Grassi 74, 20157 Milano, ITALY - Phone 0039-2
-35799541 - Fax 0039-2-38201160
APStracts 3:0151R, 1996.
Central nervous system feedback loops centered on hypothalamic neurons
control Atrial Natriuretic Peptide (ANP). We evaluated the ANP
response to arterial hypotension, isotonic blood volume expansion and
increase in plasma osmolality in 14 patients with multiple system
atrophy (MSA). Seven of the patients were characterized by a lack of
vasopressin response to hypotension (MSA-Type B), suggesting chronic
sinoaortic denervation, and seven by a preserved response (MSA-Type
A). Orthostatic hypotension decreased ANP in controls and Type A
patients, whereas ANP in Type B was not affected. Isotonic saline
infusion increased ANP and diuresis in controls and Type A patients,
whereas it did not affect ANP in Type B. Osmotic load increased
plasma osmolality and vasopressin in controls and patients and ANP in
controls and Type A, but not in Type B. In MSA patients with altered
afferent control of vasopressin, ANP secretion is not stimulated by
blood volume expansion, osmotic load, and blood pressure suggesting
that afferent excitatory control plays a role in the release of ANP.
Received 16 February 1995; accepted in final form 2 April 1996.
APS Manuscript Number R123-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 23 April 96