EFFECT OF CORTICAL STIMULATION UPON EPINEPHRINE ACTIVITY

Abstract

Electrical stimulation of the anterior sigmoid gyri of cats evoked increased epinephrine secretion, as measured by significant increases of venous blood lactic acid concentration. Stimulation of cortical vasopressor areas or their projections was followed by contraction of the sensitized, chronically denervated nictitating membrane if the adrenal glands were intact, implying an increase in circulating adrenal medullary hormones. Following stimulatation of known cortical vasodepressor areas, the previously contracted denervated nictitating membrane relaxed, suggesting a decrease in circulating adrenal medullary hormones. Evidence indicates that this resulted from inhibition of prevailing discharge in the secretory fibers to adrenal medullary cells. In electrode positions permitting stimulation of corticofugal fibers in the internal capsule, it was possible to differentiate loci giving blood pressure rise plus contraction of the denervated nictitating membrane from closely adjacent loci evoking pressor response with relaxation of the membrane. This is interpreted to mean that vasomotor and adrenal medullary secretory responses may be mediated by discrete pathways from the cortex.