Hypertension, Vol 1, 498-507, Copyright © 1979 by American Heart Association
RD Bunag and E Riley
Daily electrical stimulation of the posterior hypotalamus for 12 weeks in
awake rats caused persistent cardioacceleration but barely increased
systolic pressure. Subsequent postmortem examination showed extensive
fibrosis at sites of electrode implantation in both stimulated and
unstimulated rats. Because Folkow and Rubinstein had succeeded in elevating
blood pressure progressively by stimulating the "hypothalamic defence
area," chronic stimulation was repeated following their stereotaxic
coordinates. Systolic pressure rose but the elevation was significant only
on Weeks 8 and 10. To maintain behavioral effects during chronic
stimulation, current strengths had to be increased periodically, and
stimulated rats gained weight more rapidly than unstimulated controls. Both
these findings indicated that electrical stimulation had damaged the brain,
but since local fibrosis made histologic verification difficult, additional
experiments were done to determine if functional deficits could be
detected. Upon further hypothalamic stimulation, electrical thresholds were
higher and pressor and sympathetic nerve responses were smaller in rats
that had been stimulated chronically than in those that had not. Although
our results do not disprove the hypothesis that centrally-induced
sympathetic hyperactivity initiates hypertension, they show that blood
pressure cannot be elevated by hypothalamic stimulation alone when the
brain has been injured.
ARTICLES
Chronic hypothalamic stimulation in awake rats fails to induce hypertension
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