A mathematical model for the secretion of glucocorticoid due to human stress

To analyzing accelerated life-test data from step-stress model on changes in nitric oxide (NO) release might be responsible for the modulation by glucocorticoids of the pressor response to s.c injection of interleukin-1β (IL-1β) in humans. Treatment with Nv-nitro-L-arginine methyl ester (L-NAME, a nonspecific NO synthase inhibitor), enhanced the pressor response while attenuating the increase in plasma NOx. The result suggest that endogenous NO moderates the pressor response to IL-1β in human, and that glucocorticoids enhance the IL-1β-induced pressor response at least in part by reducing endogenous NO release, so that the blood pressure to normal level.