This project is designed to define the mechanisms by which changes in hemodynamic variables induce changes in the release of ACTH by the pituitary and in secretion of cortisol by the adrenal. Special attention is directed to the definition of the anatomical organization and physiologic control of central nervous pathways mediating release of ACTH in response to hemodynamic changes. Further attention is directed to the modulation of hemodynamic control of ACTH by other neural pathways and by humoral mechanisms, including the action of steroids, of vasopressin and of angiotensin II. Special attention is directed to the definition of temporal and quantitative features of the response of ACTH and of cortisol to hemodynamic changes and to the relating of this overall response of the system to central neural processing. Experiments utilize one hemodynamic variable used as a stimulus with control of other key hemodynamic variables within narrowly defined limits by means of computer directed closed loop automatic control. Neurophysiological techniques including electrical and chemical stimulation, single unit recording and tracing of anatomical pathway are applied in conjunction with measurements of ACTH and of cortisol by radioimmunoassay. In addition, studies are continuing to define the role of cortisol in mediation of restitution of plasma volume after hemorrhage, since through this mechanism the steroid response can modulate the hemodynamic input itself. The results of these studies will be incorporated in a comprehensive description of the function of this system, to extend previous descriptions.
NIH ExPorter
NIH ExPorter