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Endocrinology, Vol 99, 1213-1219, Copyright © 1976 by Endocrine Society
ARTICLES |
DG Ward and DS Gann
To define the role of the dorsal medulla in the control of release of ACTH, the authors stimulated electrically (30 sec, 100 muA, 50 Hz) 50 sites in the vicinity of the solitary nuclei of 11 cats anesthetized with chloralose/urethane. Responses of arterial pressure to electrical stimulation were not correlated significantly with release of ACTH. Indirect effects of changes in arterial pressure could not explain changes in release of ACTH. Concentrations of ACTH were measured by radioimmunoassay. Active areas associated with the solitary nucleus were : 1) lateral inhibitory: ventral and lateral to the solitary tract (mean delta ACTH:-153, -86, -97 pg/ml at 1.5, 3.0 and 6.0 min respectively; P less than 0.01); 2) medial inhibitory: medial dorsal motor nucleus of the vagus and extending to the midline (mean delta ACTH: -81, -107, -67 pg/ml; P less than 0.01); and 3) intermediate facilitatory: lateral nucleus intercalatus and adjacent reticular formation (mean delta ACTH: +105, +158, +4 pg/ml; P less than 0.01). The former two areas contain neurons activated by atrial stretch, and the latter area contains neurons inhibited by atrial stretch. Since changes in ACTH levels are inversely correlated with atrial stretch, the results suggest that the changes in release of ACTH are the result of direct stimulation of neural systems of the solitary nuclei mediating release of ACTH in response to hemodynamic changes.
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