Physiological role of corticotropin-releasing factor in the control of adrenocorticotropin-mediated corticosterone release from the rat adrenal gland.

摘要: Marked fluctuations in adrenal sensitivity to ACTH have been reported under both physiological (e.g. diurnal) and experimental conditions. Recently, we that immunoneutralization of CRF reduces resting corticosterone (cort) levels rats without inducing concomitant reductions plasma ACTH. We postulated an endogenous mechanism controls the In present study, this hypothesis was tested by iv infusion human (0, 1, 3, 10 ng/kg.min for 60 min) into dexamethasone-treated anaesthetized male Wistar rats. Serial blood samples were taken determination RIA (ACTHi, corti). Infusion resulted dose-dependent steady state ACTHi levels, ranging from 50-600 pg/ml, which not affected prior administration a rat monoclonal antibody (PFU 83). As expected, increase corti. PFU 83-treated rats, preinfusion corti reduced compared those immunoglobulin G-treated (7.8 +/- 1.2 vs 25.3 3.2 ng/ml). addition, responses 1 3 suppressed 83. However, at (near) maximally effective dose (10 ng/kg.min), no differences found between 83 These findings suggest results 3-fold reduction Subsequently, studied possible effects exogenous on isolated perfused gland situ. preparation, alone (1-100 pmol) or (5 fmol) did affect secretion rate flow perfusion medium through gland. when given together marked (up times) stimulation 1.7 obtained. experiments with freshly dispersed cells vitro, (1 microM) (0.1-10 nM) influence ACTH-induced secretion. It is unlikely, therefore, acts directly steroid-producing cells.(ABSTRACT TRUNCATED AT 400 WORDS)