AN ANALYSIS OF HYPOTHALAMIC CARDIOVASCULAR CONTROL

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Abstract
Stimulation of the hypothalamus of the anesthetized cat with brief repetitive shocks of moderate intensity leads, after a latency of less than 0.1 sec., to an abrupt increase in activity in sympathetic nerves to the heart and blood vessels. This activity ceases equally abruptly when stimulation is stopped and for a variable period thereafter spontaneous activity is inhibited. The delay in rise in blood pressure (1-2 secs.) and prolongation of the rise after stimulation is stopped (several secs.) result from latency and inertia of the effector, not from any corresponding delay or persistence of neural activity. An increase in intensity or frequency of hypothalamic stimulation increases the magnitude and duration of the rise in blood pressure. This increased effector response is brought about by an increase in the number of sympathetic motor neurones set into activity and by an increase in the frequency of response of each neurone. The buffer reflexes which control the spontaneous sympathetic outflow from the medullary centers also moderate the outflow induced by hypothalamic stimulation. Thus activation of the buffer afferents may inhibit all sympathetic activity induced by hypothalamic stimulation, decrease the number of responding neurones, or decrease the frequency of response of each. The frequency of firing of a sympathetic neurone in response to hypothalamic stimulation is detd. by the level of excitation maintained by the hypothalamic volleys, the time course of the recovery cycle, and the degree of activity of inhibitory afferents impinging on the medulla.

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