Explain how cortisol and epinephrine from the adrenal gland help a person to respond to stress, e.g. physical danger or surgery.

Outline:

·        Stimulation of release by stress

·        Actions on:

- metabolism

- central nervous system

- cardiovascular system

- immune system

Essay:

            Stress on the body is defined as any condition that threatens the survival of the organism or disrupts its normal functioning and activities. Stressful conditions include physical danger, fasting, infections, invasion by foreign organisms and the post-surgical period. The body is well equipped with a set of adaptations to defend itself against stress. Both the adrenal cortex and the adrenal medulla are major participants in adaptation to stress. The immune system is involved when stress is produced by foreign substances or invading organisms.

            Stress is perceived by many areas of the brain, from the cortex down to the brainstem. Afferent nerve pathways from many parts of the brain converge on the median eminence. Fibers from the amygdaloid nuclei mediate responses to emotional stresses, fear, anxiety, and apprehension. Major stresses activate CRH and ADH neurons in the paraventricular nucleus and adrenergic neurons elsewhere in the hypothalamus. The activation is mutually reinforcing, because norepinephrine increases CRH release, and CRH increases adrenergic discharge. CRH and ADH release stimulates ACTH release and ulitmately elevates plasma cortisol levels; adrenergic stimulation elevates plasma epinephrine and norepinephrine levels.

            Together, cortisol and the catecholamines increase glucose production. Catecholamines do so rapidly by activating glycogenolysis, and cortisol acts more slowly by providing amino acid substrate for gluconeoegenesis. The end result is a shift in glucose utilization toward the central nervous system and away from peripheral tissues. Epinephrine also rapidly augments free fatty acid supply to the heart and to the muscles, and cortisol facilitates this lipolytic response.

            The cardiovascular effects of epinephrine reinforces its metabolic actions. Norepinephrine acts on b₁ receptors in the sinoatrial node to increase the rate of sinus nodal discharge. It increases the permeability of cardiac muscle fibers to sodium and calcium, increasing the heart rate and force of contraction. Norepinephrine acts on a receptors on the smooth muscle of arterioles and venules, vasoconstricting them and thereby increasing blood pressure and venous return. Epinephrine acts on b₂ receptors in the coronary arteries and arteries in the liver, abdomen and muscles to cause vasodilation, increasing the blood flow through them. These changes guarantee delivery of substrate for energy production to the critical organs in the fight-or-flight situation. Cortisol augments the response of arterioles to catecholamines and decrease the synthesis of prostaglandins, a potent vasodilator. Cortisol maintains the contractility and work performance of skeletal and cardiac muscle. This inotropic action of cortisol on skeletal muscle may be exerted at the myoneural junction via an increase in acetylcholine synthesis. In addition, cortisol increases myocardial Na⁺-K⁺-ATPase and b-adrenergic receptors. These actions of cortisol helps the individual to flee from danger. However, chronic elevation of cortiso decreases muscle protein synthesis, increases muscle catabolism, and consequently reduces muscle mass and strength.

            Catecholamines exert other diverse effects. Inhibition of gastrointestinal and genitourinary motor activity, relaxation of bronchioles to prevent expiratory airway obstruction and improve gas exchange, and dilation of pupils to permit better distant vision are of benefit to the endangered individual. Catecholamines modulate ADH release. They increase renin release by stimulation of b receptors in the kidney. The increase in renin increases aldosterone secretion, which in turn enhances sodium retention.

            The neurotransmitter norepinephrine and the neuropeptide CRH can produce other adaptive responses to stress. A general state of arousal and vigilance, an activation of defensively useful behavior, and appropriate aggressiveness result from adrenergic stimuli to the pertinent brain centers. At the same time, CRH input to the hypothalamic neurons inhibits growth hormone and gonadotropin release, as well as sexual activity because these actions are not useful during stress. In addition, CRH inhibits appetite and feeding behavior.

            During injury, a variety of cytokines are release at the site of injury to stimulate cellular and humoral defenses that repel, neutralize, or eliminate harmful organisms or foreign molecules. However, a balance is needed between these useful responses and their possible counterproductive systemic spread. If plasma cytokine concentrations become greatly elevated, they stimulate CRH release, which ultimately raises plasma cortisol. As the level of plasma cortisol becomes progressively elevated, the production of these same cytokines is inhibited.

            In short, the hypothalamic CRH-pituitary ACTH-adrenal cortisol axis and the sympathetic nervous system operate jointly in adaptation to stress. They reinforce each other’s actions to promote life-saving behavior and inhibit activities that divert individuals and their resources from defensive responses to danger.