Figure 1 shows two pathways describing the con sequences of exposure to stress. The left-hand “stress” column is titled “Loss of control” which can lead to a long-standing circumstance (months and/or years) that includes extensive secretion of ACTH, which will elevate the circulating concentrations of corticosterone. The right-hand Stress column is titled Threat to control. Depending on the outcome of the Active (fight f light), there are two outcome paths (brown color) titled Control or Striving. It is important to emphasize that these two pathways sometimes operate simultaneously, but they can also be dissociated from one another, especially when the individual is confronted with an emotionally stressful situation and copes on different levels.

Fig1. A defense reaction is activated when the organism is exposed to stress, but remains in control (see left column). With the loss of control there is activation of the hypothalamus-pituitary-adrenal axis, and the gonadotrophic species preservative system shuts down. Visceral fat accumulates in a Cushingoid distribution and there is a shift from active physical defense to a passive nonaggressive coping style. Reproduced by permission from J.P. Henry (1993) in Biological Basis of the Stress Response. NIPS 8:69–73.

The sympathetic adrenomedullary pathway (right hand side) is activated when a fight or flight response is issued to a specific challenge. On the other hand, the humoral pathway (left-hand side), ending in cortisol release from the adrenal gland, is also operative when the individual becomes immobile, passive, and depressed as loss of control is perceived. A chronic emotional reaction of passivity and defeat to a stressful situation can produce dire consequences, as the adrenal hypertrophy and levels of cortisol continue to increase. This can generate a Cushingoid-like bodily reaction in which visceral fat accumulates and blood pressure becomes elevated, and arteriosclerosis and type II diabetes eventually develop. Sequential episodes of elevated glucocorticoids cause sufficient repression of glucose uptake in peripheral cells to involve insulin release from the β-cells of the pancreas.

Eventually, chronic repetitions of this scenario can lead to exhaustion of the β-cells’ ability to produce and secrete insulin. The metabolic changes in the organism induced by elevated levels of glucocorticoids, such as cortisol, are mediated by the amount of available glucocorticoid receptor proteins located in the cytoplasm of target tissues. Very important organs are liver, lymphocytes (including thymus cells), adipose cells, kidney, anterior pituitary, and various parts of the brain. Some of the effects of cortisol on tissues of normal or adrenalectomized rats are shown in Table 1.

Table1. Biological Effects of Cortisol

Glucocorticoids are secreted in large amounts in humans, up to 25 mg or more per day, which constitutes a major chemical response of the body to stress. A person undergoing long-term stress will have higher amounts of cortisol circulating in the bloodstream than the unstressed person. The ability of cortisol to act on many of the tissues of the body is determined by the distribution and number of glucocorticoid nuclear receptors present in the cell of a particular tissue. The adult rat liver contains about 65,000 receptor molecules per cell which bind corticosterone, which is the principal glucocorticoid in the rat. Other important targets are the lymphoid cells, thymus gland, and kidney. Many other tissues appear to have enough receptor molecules to provide a response to stress, especially if it is long-term. In fact, most tissues of humans and animals or of cells in tissue culture seem to contain measurable amounts of the glucocorticoid receptor, making it theoretically possible for nearly all tissues of the body to be affected by stress.

Long-term stress may be distinguished from short term stress, often referred to as “alarm” or “fright.” In short-term stress, the minute-to-minute changes in metabolism are under the control of catecholamine hormones, primarily epinephrine, secreted by the adrenal medulla. The secretion of epinephrine is in turn controlled by the autonomic nervous system. Both stresses, long- or short-term, lead to the release of glucocorticoids.

Glucocorticoids are so named because the steroid hormone influences the polymerization of glucose into the form of glucose macromolecules termed glycogen. This glycogen is an insurance policy that can be utilized on a minute-to-minute basis when the breakdown of glycogen is necessary to enable escape or survive the “fight or flight” or provide “nervous energy.” Epinephrine is the primary hormonal signal that instantly activates the release of glucose molecules from the stored glycogen. Many other hormones are involved in stress, including glucagon, growth hormone, prolactin, β-endorphin, vasopressin, angiotensin II, and prostaglandins.

Thus it is possible to classify two types of stressors. One class includes responses that are in effect for a long period of time. These include intensive cold, pro longed loud noise, serious injury, burns, surgery, and significant changes in the environment. These stressful circumstances necessitate the “rapid” response adaptation. If adaptation does not occur, the second type of stressors lasts only for a very short interval. The alarm emergency or shorter term stressor would be an event of a surprise nature, such as fright induced by a specific happening. This type of stressor would primarily evoke the secretion of epinephrine (and norepinephrine) from the adrenal medulla, as well as cortisol secretion from the adrenal cortex. Both types usually occur simultaneously; one change in operation does not preclude the utilization of the other pathway. There are, however, certain conditions that can cause the pathways to operate separately. The sympathetic system generating epinephrine and norepinephrine is activated when the organism attempts to escape from or deal with the environmental challenge or the flight or flight response (see the right arm of Figure 2 in section V.B). When the organism becomes immobile or passive, the adrenocortical axis is preferentially activated.

Fig2. Example of pigmentation disorders associated with idiopathic Addison’s disease. The hand on the left highlights the skin pigmentation problems experienced by a patient with Addison’s disease. The hand on the right side is from a healthy person. Reproduced from Ezrin, C., Godden, J. O., Volpe, R. and Wilson, R. (Eds) (1973). Systematic Endocrinology, p. 178. Harper & Row, New York.

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