The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole.

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Plasma levels of corticosterone are often used as a measure of ''stress'' in wild animal populations. However, we lack conclusive evidence that different stress levels reflect different survival probabilities between populations. Galá pagos marine iguanas offer an ideal test case because island populations are affected differently by recurring El Niñ o famine events, and population-level survival can be quantified by counting iguanas locally. We surveyed corticosterone levels in six populations during the 1998 El Niñ o famine and the 1999 La Niñ a feast period. Iguanas had higher baseline and handling stress-induced corticosterone concentrations during famine than feast conditions. Corticosterone levels differed between islands and predicted survival through an El Niñ o period. However, among individuals, baseline corticosterone was only elevated when body condition dropped below a critical threshold. Thus, the population-level corticosterone response was variable but nevertheless predicted overall population health. Our results lend support to the use of corticosterone as a rapid quantitative predictor of survival in wild animal populations.

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(Sturnus vulgaris) to test whether corticosterone responses differed in birds held under normal laboratory conditions or conditions of chronic stress. Surprisingly, both basal corticosterone concentrations and corticosterone responses to acute stress were significantly reduced when birds were chronically stressed. To determine the mechanism underlying this reduced response, animals under both conditions were injected with lactated Ringer's solution (control), adrenocorticotropin (ACTH), arginine vasotocin (AVT), or dexamethasone (DEX). ACTH increased corticosterone concentrations above stress-induced levels in both cases, although maximum responses were lower in chronically stressed birds. AVT did not augment the corticosterone response under nonchronically stressed conditions, but it did under chronically stressed conditions. DEX reduced maximal corticosterone concentrations in both cases. Neither ovine nor rat corticotropin-releasing factor (CRF) altered normal stress responses. These data indicate that changes in responsiveness of the hypothalamic-pituitary-adrenal axis to ACTH and AVT serve to downregulate corticosterone responses during chronic stress. Furthermore, these data lead to the following hypothesis: ACTH output from the pituitary limits maximum corticosterone concentrations under normal conditions, but reduced AVT release from the hypothalamus regulates lower corticosterone concentrations under chronic stress conditions. environmental stress; negative feedback; hypothalamic-pituitary-adrenal axis; conservation GLUCOCORTICOIDS ARE STEROID hormones released from adrenal tissue in response to stressful stimuli. Upon perception of stress, the avian hypothalamus is activated to secrete arginine vasotocin (AVT, a congener of the mammalian arginine vasopressin) and corticotropin-releasing factor (CRF), which stimulate the pituitary to release adrenocorticotropin (ACTH), in turn, causing the release of glucocorticoids from the adrenals (7,8). This pathway constitutes the hypothalamic-pituitaryadrenal (HPA) axis, and its activation is one component of the physiological stress response. This response is believed to be aimed at maintaining or restoring homeostasis, thereby helping the animal to survive a stressful episode (45, 50). The primary avian glucocorticoid is corticosterone (CORT) (22).The presumed benefits of an acute activation of the HPA axis contrast with chronic activation. Various deleterious effects of chronic CORT elevation have been documented in many species, including suppression of reproductive function and behavior, immune system suppression, muscle wasting, growth suppression, and neuronal cell death (45, 49). Chronic stress generally produces chronic elevations in baseline CORT concentrations. However, studies of chronically stressed rats indicate that facilitation of the HPA axis takes place to maintain responsiveness to acute stressors (11,13,25), perhaps by increasing the role of vasopressin over CRF in the release of ACTH (1, 16, 17). Therefore, animals must avoid chronic stress ...