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Am J Physiol Heart Circ Physiol 270: H2143-H2148, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 270, Issue 6 2143-H2148, Copyright © 1996 by American Physiological Society

ARTICLES

Sympathovagal interplay in the control of overall blood pressure variability in unanesthetized rats

A. U. Ferrari, C. Franzelli, A. Daffonchio, S. Perlini and M. Dirienzo
Centro di Fisiologia Clinica e Ipertensione, Universita di Milano, Italy.

The role of sympathetic and parasympathetic influences in the control of overall blood pressure variability was studied in chronically instrumented, freely behaving Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) subjected to sympathectomy by 6-hydroxydopamine (100 micrograms/kg ip) twice in 1 wk (effectiveness verified by abolition of pressor and tachycardic response to tyramine, 150 mg/kg i.v.) and/or to cholinergic blockade by atropine (0.7 mg/kg 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 with the vehicle-treated controls, sympathectomized rats had much larger blood pressure variability (WKY, +61%, SHR, +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 WKY and 28% in SHR (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, 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; and 3) chronic hypertension fails to alter these cardiovascular regulatory mechanisms.


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