Sympatho-vagal interplay in the control of overall blood pressure
variability in unanesthetized normotensive and hypertensive
rats..
Ferrari, Alberto U., Cristina Franzelli, Anna Daffonchio, Stefano
Perlini, Marco Dirienzo.
Centro di Fisiologia Clinica e Ipertensione, Cattedra di
Fisiopatologia Applicata, Istituto di Clinica Medica Generale e
Terapia Medica, Universit[grave]a di Milano; Ospedale Maggiore and
C.N.R., Milano; #LaRC, Centro di Bioingegneria, Politecnico di
Milano; Divisione di Cardioribilitazione, Ospedale di Seregno
Az/U.S.S.L. 30, Desio, Italy
APStracts 3:0023H, 1996.
The role of sympathetic and parasympathetic influences in the control
of overall blood pressure variability was studied in chronically
instrumented, freely-behaving Wistar-Kyoto and spontaneously
hypertensive rats subjected to sympathectomy by 6-hydroxydopamine,
150 mg.kg-1 i.p. twice in one week (effectiveness verified by
abolition of pressor and tachycardic response to tyramine, 150 mg.kg
-1 i.v.) and/or to cholinergic blockade by atropine, 0.7 mg.kg-1 i.v.
Overall heart rate and blood pressure variabilities were measured as
variation coefficients computed beat-to-beat on 90 min blood pressure
recordings. As compared to the vehicle-treated controls,
sympathectomized rats had much larger blood pressure variability
(Wistar-Kyoto rats +61%, spontaneously hypertensive rats +86%, both
p<0.01). Cholinergic blockade superimposed to sympathectomy
caused heart rate variability to markedly fall and the already
augmented blood pressure variability to further rise 47% in Wistar
-Kyoto and 28% in spontaneously hypertensive rats (both p<0.01).
Prolonged observation of the animals revealed the systematic
occurrence of rapid blood pressure falls occurring at the onset of
locomotor activity, this accounting for a substantial fraction of the
sympathectomy-related increase in blood pressure variability. It is
concluded that: 1) under undisturbed, daily life conditions
sympathetic influences oppose blood pressure variations, presumably
by adjusting their vasoconstrictor influences to compensate for the
metabolic vasodilation occurring in functionally active tissues; 2)
when sympathetic vascular control is lost, vagally-mediated heart
rate variations oppose the rise in blood pressure variability,
possibly via rapid changes in cardiac output that partly offset the
fluctuations in total peripheral resistance; 3) chronic hypertension
fails to alter these cardiovascular regulatory mechanisms.
Received 24 February 1995; accepted in final form 13 November
1995.
APS Manuscript Number H178-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96