Adrenal responses to stress

Abstract

Based on concepts proposed by Langley, Cannon, and Selye, adrenal responses to stress occur in a syndrome that reflects activation of the sympathoadrenal system and hypothalamic–pituitary–adrenocortical (HPA) axis; and a "stress syndrome" maintains homeostasis in emergencies such as "fight or flight" situations, but if the stress response is excessive or prolonged then any of a variety of clinical disorders can arise. The idea of a unitary sympathoadrenal system does not account for evidence that different stressors elicit different patterns of autonomic responses, with exposure to some stressors differentially affecting sympathetic noradrenergic and adrenomedullary hormonal activities. Instead, adrenomedullary responses to stressors are more closely tied to adrenocortical than to sympathetic noradrenergic responses. Distress involves concurrent activation of the HPA and adrenomedullary neuroendocrine systems.

Fig. 1

A physiological homeostatic system. As the level of the monitored variable changes, afferent information is compared with a set point or other algorithm for responding, and the sensed discrepancy leads to altered activities of effectors. Note the odd number of (−) signs, indicating a negative feedback loop. In response to a continuous perturbation, the level of the monitored variable reaches an apparent steady state

Fig. 2

Compensatory activation. One advantage of multiple effectors is compensatory activation of alternative effectors if one effector fails, enabling control of the monitored variable. For instance, thyroidectomy augments sympathetic nervous system (SNS) responses to cold exposure

Fig. 3

Effector sharing. Sharing of an effector by multiple homeostats can explain unpredicted consequences and syndromic features of disease processes. For instance, in heart failure, decreased aortic filling increases levels of vasopressin (AVP), which, as the anti-diuretic hormone, promotes retention of free water, explaining hyponatremia attending heart failure

Fig. 4

Systems definitions of stress and allostatic load. In stress, the organism senses a discrepancy between afferent information about a monitored variable and a set point and other instructions for responding, altering activities of effectors to decrease the discrepancy. Allostatic load reflects wear and tear, which, if sustained and substantial enough, decreases effector efficiency, further activating the effector and accelerating wear and tear. Allostatic load can therefore eventuate in a destabilizing and pathologic positive feedback loop

Fig. 5

Mean values across 15 different stressors for plasma levels of a epinephrine (EPI) and corticotrophin (ACTH); b EPI and norepinephrine (NE); and c NE and ACTH. Dashed lines indicate lines of best fit