Chronic hypothalamic stimulation in awake rats fails to induce hypertension.
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.
D000818:Animals; D001522:Behavior, Animal; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight; D002320:Cardiovascular Physiological Phenomena; D005260:Female; D006339:Heart Rate; D006973:Hypertension / Q000209:etiology*; D007031:Hypothalamus / Q000502:physiology*; D007034:Hypothalamus, Posterior / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D013997:Time Factors
D009638:Norepinephrine