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It has been suggested that hyperinsulinemia per se may affect the levels of some counterregulatory hormones in the absence of hypoglycemia. We studied the effect of graded hyperinsulinemia and concomitant increased glucose metabolism on the levels of counterregulatory hormones by means of the 5-step sequential hyperinsulinemic euglycemic clamp technique, combined with [3-3H]-glucose infusion, in conscious rats. Insulin infusion rates (IIR) of 0, 0.5, 1, 3, and 16 mU/min, resulted in steady-state plasma insulin levels (mean +/- SEM) of 24 +/- 4, 44 +/- 3, 98 +/- 8, 418 +/- 48, and 6626 +/- 361 microU/ml, peripheral glucose uptake (PGU) of 3.1 +/- 0.2, 3.6 +/- 0.3, 5.4 +/- 0.3, 9.2 +/- 0.4, and 12.4 +/- 0.2 mg/min and hepatic glucose production (HGP) of 3.1 +/- 0.2, 2.4 +/- 0.4, 0.8 +/- 0.3, -0.1 +/- 0.2, and -0.5 +/- 0.3 mg/min, respectively. Plasma glucagon levels were half maximally suppressed between IIRs of 0.5 and 1 mU/min and maximally suppressed at 3 mU/min. The suppression exactly paralleled the inhibition of HGP (r = 0.87 +/- 0.04, p < 0.02) but not the stimulation of PGU (r = -0.66 +/- 0.12, p = NS). This suggests that the inhibition of HGP by insulin is at least partially mediated by a simultaneous suppression of plasma glucagon levels. The adrenal hormones corticosterone and epinephrine were not influenced during the clamp.(ABSTRACT TRUNCATED AT 250 WORDS)

In an attempt to assess possible discomfort in rats subjected to orbital puncture while under diethyl-ether anaesthesia, their endocrine stress response was determined. Concentrations of corticosterone, adrenaline and noradrenaline were measured in plasma obtained via a jugular catheter from rats subjected to diethyl-ether anaesthesia with or without orbital puncture. No statistically significant differences were found between the punctured and non-punctured rats as to peak levels of plasma corticosterone and adrenaline as well as for the times required by the increased concentrations to return to baseline values. The rate by which the plasma noradrenaline level returned to baseline values was somewhat decreased by orbital puncture. Diethyl-ether anaesthesia alone produced a marked endocrine response when compared with handling and novelty stress associated with the induction of anaesthesia. It is concluded that diethyl-ether anaesthesia causes pronounced increases in the plasma levels of the selected stress hormones and that orbital puncture does not amplify this response. It is suggested that diethyl-ether anaesthesia masks any effects of orbital puncture.

Plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) concentrations were determined in rats before, during and after 15-min exposure to a constantly electrified (2 mA) or nonelectrified prod which was mounted on the wall of the home cage either with or without bedding material on the floor. Concomitantly, exploration of the prod, freezing and prod-burying behavior were recorded. Both in the presence and absence of bedding material, rats explored the nonelectrified prod and showed a small increase in plasma NA and CS contents. Exploration of the prod was strongly reduced when the prod was electrified. In the presence of bedding material, shocked rats typically displayed burying behavior (active avoidance), whereas in the absence of bedding (i.e., burying option eliminated) shocked rats engaged in freezing behavior (passive avoidance). The passive avoidance situation was accompanied by larger A and CS increases but a lower NA rise as compared to the hormonal responses associated with the active avoidance situation. Administration of the anxiolytic chlordiazepoxide (CDP; 9 mg/kg intragastrically) attenuated the shock-induced suppression of prod exploration, decreased prod-burying behavior but, paradoxically, increased freezing behavior. Irrespective of bedding condition, the prod shock-induced elevations in plasma CS and A contents were completely abolished in CDP-treated rats. The rise in plasma NA was attenuated only in CDP-treated rats tested on a bedding-floor. The results indicate that passive (e.g., freezing) and active (e.g., burying) behavioral coping are each accompanied by specific and dissociated patterns of neurosympathetic, adrenomedullary and adrenocortical outflow. CDP-treatment shifts an animal's behavioral coping style from an active to a passive form of avoidance responding, but abolishes the accompanying adrenocortical and adrenomedullary activation.

Plasma noradrenaline (NA), adrenaline (A), corticosterone (CS) and glucose concentrations were determined in blood frequently sampled via a cardiac catheter from freely behaving rats exposed to five successive trials of water-immersion stress (WIS) with an interval between successive trials (interstressor interval; ISI) of either 24 hr or 72 hr. The first, acute exposure to WIS was accompanied by increased levels of plasma NA, A, CS and glucose which were substantially higher than those associated with handling or placement into a new cage. The magnitudes of the WIS-induced plasma NA, A, CS and glucose responses gradually declined across trials. However, five WIS exposures at a 24-hr ISI resulted in a faster and greater decrement of the plasma A, CS and glucose responses than five exposures at a 72-hr ISI. The data indicate that frequency of stressor presentation (i.e., length of interstressor interval) affects the adaptation pattern of neuroendocrine and metabolic responses to chronic intermittent stress. This finding supports the hypothesis that neuroendocrine adaptation to stress is (at least partly) similar to the process of behavioral or neurophysiological habituation to a sensory stimulus.

Plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) concentrations were determined simultaneously in permanently heart-cannulated rats before and during the performance of reinforced and nonreinforced (extinguished) operant behavior. Shortly before the experimental food-reinforced (VI 15-sec schedule) lever-pressing task, anticipatory elevations of plasma NA and CS contents were observed. During reinforced lever responding plasma NA increased, A did not change and CS declined. Extinction was associated with a transient increase in A, decreasing NA and elevated CS concentrations. In addition, a relationship was found between individual lever-pressing rate, neurosympathetic and adrenomedullary reactivity and the degree of schedule-induced polydipsia. The results indicate that presence and absence of expected behavioral consequences (controllability and loss of control, respectively) are attended by selective, but highly dissociated patterns of neurosympathetic, adrenomedullary and adrenocortical output. Collectively, the findings reinforce the concept that distinctive emotional and/or motivational states are associated with different patterns of neuroendocrine responses. The reactivity of the sympathoadrenomedullary component is heavily dependent upon a rat's individual behavioral strategy.

Plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) concentrations were determined in blood frequently sampled via a cardiac catheter from freely moving rats exposed to three successive trials of white-noise stimulation (10 min, 100 dBA) with an intertrial interval of 30 min. During the sampling period, behavioral activities of the rats were recorded. It was demonstrated that the first exposure to noise induced a specific temporal pattern of neuroendocrine changes: Plasma A and NA contents increased rapidly and peaked early after stimulus onset but their peak-latencies were different (1 and 5 min, respectively). Noise offset was followed by quick return to basal levels. The changes in plasma CS concentrations were considerably slower in onset and slower in decline. The second and third exposure to this type of stressor resulted in attenuated hormonal responses and a reduced decrement of the NA/A-ratio, concurrent with a gradually less intense behavioral reaction. This differential pattern of plasma NA, A and CS responses following repetitive exposure to identical stressors, referred to as adaptation, is discussed with regard to the biochemical changes at various levels of the neuroendocrine systems involved.

Plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) increases were determined in individual rats subjected to either 20 regularly or irregularly scheduled white-noise stimulations (4 min, 100 dBA). Blood was frequently sampled during the first and twentieth noise exposure, and during a reexposure after 24 hr. During the sampling periods, behavioral activities of the rats were recorded. The initial noise-induced CS release was partially reduced following the regular noise presentations. The increase after irregular presentations remained high. The difference in adrenocortical responsiveness between regular and irregular exposure persisted for 24 hr. The NA response to noise was partially attenuated following irregular administration of noise. However, regular exposure produced increased NA levels prior to noise presentation and a subsequent decrease during stimulation. After 24 hr, noise evoked an exaggerated initial NA release in the regular group. The noise-elicited rise in A was completely abolished after 20 noise presentations irrespective of whether these were applied regularly or irregularly. Reexposure after 24 hr evoked again a significant A response in both groups. No differences were observed in the habituation pattern of behavioral reactions among the regular and irregular groups. The results show that the sympathetic neural, adrenomedullary and adrenocortical systems differ in degree and speed of adaptation to intermittent stressful stimuli and in sensitivity to the predictability of stressors.

Plasma noradrenaline (NA), adrenaline (A), corticosterone (CS) and glucose concentrations were determined in blood sampled via a cardiac catheter from freely moving male rats under ad lib fed and 24 hr food deprived conditions using a repeated measures within-subject design. Resting plasma NA and glucose levels were lower in the fasted condition as compared to the fed situation. One day of refeeding reinstated the decreased NA and glucose values to prefasting level. Exposing 24 hr food deprived animals to the psychological stress of a novel environment resulted in larger NA and glucose increases, an unchanged A release and a lower CS rise in comparison with the responses during the free feeding state. The results show the usefulness of a within-subject design to detect subtle changes in plasma NA contents. Additionally, the data support the concept of selective control of the sympathetic nervous system and adrenal medullae. It is argued that hypothalamic noradrenergic mechanisms may be linked to the fasting-induced effects on the sympatho-adrenal system.

Plasma noradrenaline (NA), adrenaline (A) and corticosterone (CS) concentrations were determined in blood samples taken once every hour during a 12-hr light/12-hr dark period from freely moving rats with a permanent heart cannula. Before, during and shortly after each blood sampling, behavioral activity was recorded. All rats exhibited a very pronounced peak in CS concentrations at the end of the light period, indicating normal circadian rhythmicity. Plasma NA and A contents varied significantly over the 24-hr sampling period. During nighttime, the behaviorally active phase, mean levels of circulating A and NA were significantly higher than during daytime resting period. Significant correlations between the daily NA, A and behavioral activity patterns were found only when uncorrected data were considered. In contrast, no significant correlations were found for values corrected for circadian trends, indicating that circadian patterns of NA, A and behavioral activity rather than their short-term fluctuations are similar. It is concluded that the circadian variations in plasma NA and A reflect a common activation of both the neural and adrenomedullary parts of the sympathetic autonomic nervous system, most likely associated with the daily patterning of behavior activities. On short-term basis through the day however, a dissociation between these two parts can occur suggesting separate regulating mechanisms for the fine tuning of physiological processes.