Vasopressin infusion has been shown to decrease plasma adrenocorticotropic hormone (ACTH) concentration and transiently increase plasma cortisol concentration in conscious dogs. In the present study, one experiment tested the hypothesis that vasopressin infusion decreases ACTH by activation of a V1 receptor mechanism, e.g., by increasing atrial pressures and stimulating the low-pressure baroreceptor reflex. Administration of a vasopressin V1 antagonist eliminated the increases in atrial pressure and decreases in heart rate with vasopressin infusion (1 ng · kg-1 · min-1), as it eliminated the decrease in ACTH, which is consistent with baroreflex-mediated inhibition of ACTH by vasopressin. A second experiment evaluated the role of ACTH in the increase in glucocorticoids. Dexamethasone pretreatment, which inhibits ACTH secretion, abolished the increase in glucocorticoid concentration with vasopressin infusion, indicating that ACTH is necessary for the glucocorticoid response. A third experiment was performed to determine whether the glucocorticoid response could be restored in dexamethasone-treated dogs, when ACTH concentration was maintained near control levels by intravenous infusion of synthetic α-ACTH-(1-24) (0.3 ng · kg-1 · min-1). In these dogs, vasopressin infusion produced a sustained increase in plasma glucocorticoid concentration from 22 ± 3 to 49 ± 8 ng/ml (P < 0.001). Infusing higher levels of ACTH (0.5 ng · kg-1 · min-1) enhanced basal glucocorticoid levels but did not enhance the response to vasopressin. Vasopressin infusion did not alter clearance of glucocorticoids. Collectively, these results suggest that vasopressin directly stimulates adrenal glucocorticoid production, provided that background levels of ACTH are present.
|Original language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|State||Published - Jan 1 1989|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Physiology (medical)