The onset of a acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of epinephrine and to a lesser extent norepinephrine from the medulla of the adrenal glands

The release is triggered by in event of acute stress is acetylcholine released from pre-ganglionic sympathetic nerves. These catecholamine hormones release in event of acute stress facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels in many parts of the body - but not in muscles (vasodilation), brain, lungs and heart - and tightening muscles. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviors often related to combat or escape.

Normally, when a person is in a serene, unstimulated state, the "firing" of neurons in the locus ceruleus is minimal. A novel stimulus in event of acute stress, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signaling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes alert and attentive to the environment.

Too much of the wrong stimuli release at time of acute stress can be a bad thing causing heart disease, sexual dysfunction, high blood pressure, and immune deficiencies.If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system in event of acute stress . The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centers, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal

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