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Sections of Physiology/Biophysics and Surgery, Brown University, Rhode Island Hospital Providence, Rhode Island 02902
Address correspondence and requests for reprints to: Drew E. Carlson, Ph.D., Nursing Arts Building, Room 217, Rhode Island Hospital, 593 Eddy Street, Providence, Rhode Island 02902.
Abstract
To determine if arginine vasopressin (AVP) is involved in the response of ACTH and cortisol (F) to hemorrhage, we examined the effect of injections of AVP-antiserum into the third ventricle in chronically prepared awake cats. Cats were trained to remain unrestrained in a cardboard box. Cats were prepared under halothane and nitrous oxide with aseptic technique. Two to 3 days later, experiments began. Antiserum (5 µl) to AVP or to oxytocin (OXY) as a control was given 26 min before hemorrhage conducted over 3 min. Thirty minutes after hemorrhage, reinfusion was conducted over 3 min. Each cat received each antiserum in randomized sequence 2–3 days apart. Plasma ACTH and F were measured by RIA. Data were analyzed statistically by analysis of variance. In 12 experiments in 6 cats, ACTH and F increased significantly with 10 ml/kg hemorrhage (P < 0.01) and to the same extent (P > 0.1) after either antiserum. In 20 additional experiments in 10 cats, a submaximal dose of dexamethasone was administered sc 2–3 h before hemorrhage of 15 or 17.5 ml/kg. Under this circumstance, ACTH increased significantly (P < 0.05) after anti-OXY, but not after anti-AVP (P > 0.2) so that during hemorrhage the values of ACTH differed significantly (P < 0.025). F increased significantly more after anti-OXY than after anti-AVP (P < 0.025). Changes in arterial pressure, heart rate, and plasma glucose with or without pretreatment with dexamethasone did not differ between groups. Changes in F and ACTH in cats receiving sham injections did not differ from those after anti-OXY. These findings suggest that normally a corticotropinreleasing factor (CRF) or factors act independently of AVP to mediate the response to hemorrhage. However, in the presence of steroid feedback by dexamethasone, the release or action of this CRF(s) is suppressed so that AVP is necessary for a full response. As has been proposed previously by others, AVP could potentiate the action of other CRFs, stimulate their release, or act as a CRF. (Endocrinology 114: 317, 1984)
Footnotes
* This work was supported in part by NIH Grant AM-26831. Antisera to AVP and to oxytocin were raised in rabbits by Dr. Alan Robinson with the support of NIH Grant AM-16166.
Received March 17, 1983.
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