The adrenal medulla is GIGANTIC. It’s the largest sympathetic ganglia. The cells are made of modified neurons that have short axons and no nerve processes. The adrenal cortex is an endocrine organ and the outer layer is the adrenal cortex while the inner layer is the medulla. When stimulated by preganglionic sympathetic fibers from T8-L1, they secrete large quantities of the excitatory hormones norepinephrine and epinephrine (adrenaline) into nearby capillaries. When these two hormones are released in the blood they amplify all of this fight or flight stuff to give you more energy.
In general, circulating epinephrine and norepinephrine released from the adrenal medulla have the same effects on target organs as direct stimulation by sympathetic nerves , although their effect is longer lasting. Additionally, of course, circulating hormones can cause effects in cells and tissues that are not directly innervated. The physiologic consequences of medullary catecholamine release are justifiably framed as responses which aid in dealing with stress. These effects can be predicted to some degree by imagining what would be needed if, for example, you were trapped in Jurassic Park when the power went off. A listing of some major effects mediated by epinephrine and norepinephrine are:
Primary aldosteronism is characterized by high blood pressure, caused by increased retention of salt and water by the kidneys, and low serum potassium concentrations (hypokalemia), caused by excess excretion of potassium in the urine. The symptoms and signs of aldosterone excess include not only hypertension but also muscle weakness and cramps and increased thirst and urination. Primary aldosteronism is usually caused by a benign adrenal tumour (adenoma), but some patients have hyperplasia of both adrenal glands. Successful removal of the adrenal tumour usually results in reduction in blood pressure and cessation of potassium loss; patients with bilateral adrenal hyperplasia are treated with antihypertensive drugs.