Essential hypertension, while considered to be idiopathic, may be due to a variety of physiologic and/or psychologic factors, including stress. A possible mechanism for stress-induced hypertension is the inhibition of prostaglandin (PG) synthesis by the release of corticoids in the stereotypical stress response. PGI2 and PGE2, acting as vasodilators are important antagonists to the pressor effects of norepinephrine. However, a decreased synthesis of these PGs due to higher cortisol levels associated with stress, would negate their vasodilatory action, thus favoring vasoconstriction due to vascular suprasensitivity to norepinephrine. PGF2 alpha, a vasoconstrictor thought to be synthesized in the brain in response to a stressor, may also play a key role in the pathogenesis of hypertension.