ABSTRACT
The role of an intact locus coeruleus (LC) noradrenergic system for the central effects of corticotropin-releasing factor (CRF) was studied. Rats were treated with N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride (DSP-4), a highly selective noradrenergic neurotoxin permanently affecting mainly the LC system. This procedure did not affect the activation of the sympathetic nervous system, as measured by plasma catecholamine levels, after either intracerebroventricular (ICV) or intraperitoneal (IP) administration of 8-micrograms CRF. Neither was the increased emotionality seen in an open field test after ICV injection of CRF altered. However, the ulceroprotective effect of 8-micrograms CRF ICV during a 2-hr water restraint stress was significantly antagonized by pretreatment with DSP-4, while CRF did exhibit an ulceroprotective effect after IP administration to DSP-4-treated animals. Our data indicate that the ulceroprotective effect of CRF under restraint stress is, at least partly, dependent on an intact locus coeruleus noradrenergic system.
Subject(s)
Arousal/physiology , Autonomic Nervous System/physiology , Corticotropin-Releasing Hormone/physiology , Hypothalamo-Hypophyseal System/physiology , Locus Coeruleus/physiology , Norepinephrine/physiology , Pituitary-Adrenal System/physiology , Receptors, Adrenergic/physiology , Animals , Corticosterone/blood , Exploratory Behavior/physiology , Gastric Mucosa/pathology , Male , Motor Activity/physiology , Orientation/physiology , Rats , Stomach/innervation , Stomach Ulcer/pathologyABSTRACT
Ten healthy female subjects performed maximum exercise on a bicycle in an altitude chamber during normoxia and hypobaric hypoxia simulating altitudes of 2,450, 3,700 and 4,600 m. The increases in systolic blood pressure responses were reduced with the degree of hypobaric hypoxia, whereas heart rate and diastolic pressure responses were unchanged. The increases in blood levels of aldosterone, plasma renin activity, adrenaline, noradrenaline, neuropeptide-Y and vasoactive intestinal peptide were similar at the different simulated altitudes. Angiotensin-converting enzyme and vasoactive intestinal peptide levels were not affected by hypoxia or maximum exercise. The present results suggest that the decreases in systolic blood pressure responses during hypobaric hypoxia could not be explained by altered responses of the measured vasoactive substances from the renin-angiotensin, gastrointestinal, and autonomic nervous systems.
