Another important aspect to consider is how your current medications might be affecting your adrenals in a negative way. It’s possible that adrenal insufficiency can develop when a person taking glucocorticoid hormones (like prednisone) for a long time, which act similarly to cortisol, suddenly stops taking those medications. If you’re on any prescriptions for treating inflammatory illnesses like rheumatoid arthritis, asthma or ulcerative colitis , talk to your doctor about how to adjust your dosage appropriately before changing them yourself since these can lower ACTH and cortisol.
Catecholamines are produced in chromaffin cells in the medulla of the adrenal gland, from tyrosine , a non-essential amino acid derived from food or produced from phenylalanine in the liver. The enzyme tyrosine hydroxylase converts tyrosine to L-DOPA in the first step of catecholamine synthesis. L-DOPA is then converted to dopamine before it can be turned into noradrenaline. In the cytosol , noradrenaline is converted to epinephrine by the enzyme phenylethanolamine N-methyltransferase (PNMT) and stored in granules. Glucocorticoids produced in the adrenal cortex stimulate the synthesis of catecholamines by increasing the levels of tyrosine hydroxylase and PNMT.  
While secondary or tertiary adrenal insufficiency (isolated glucocorticoid deficiency) does not lead to volume depletion, it decreases vascular tone, which leads to hypotension. Thus, adrenal crisis occurs less frequently in patients with secondary or tertiary adrenal insufficiency. When they do have adrenal crisis, it tends to be during acute stress, or with acute cortisol deficiency due to pituitary infarction or after surgical cure of Cushing's syndrome. (See "Clinical manifestations of adrenal insufficiency in adults", section on 'Secondary/tertiary adrenal insufficiency' .)