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Differential glucocorticoid effects on catecholamine responses to stress
1Baker Medical Research Institute, Prahran, Victoria, Australia.
The American Journal of Physiology
|January 1, 1994
Summary
Glucocorticoids, like cortisol, do not affect norepinephrine (NE) release during stress. However, they do influence epinephrine (Epi) release, with different mechanisms observed for audiovisual versus hypoglycemic stress.
Area of Science:
- Neuroendocrinology
- Stress Physiology
Background:
- Limited research exists on the interplay between glucocorticoid and catecholamine stress responses.
- Understanding these interactions is crucial for comprehending the body's adaptation to diverse stressors.
Purpose of the Study:
- To investigate the influence of glucocorticoids on adrenocorticotropic hormone (ACTH), cortisol (F), norepinephrine (NE), and epinephrine (Epi) release during acute stress.
- To differentiate the catecholamine responses to audiovisual and hypoglycemic stress and their modulation by glucocorticoids.
Main Methods:
- Plasma levels of ACTH, F, NE, and Epi were measured in sheep.
- Sheep were pretreated with cortisol, dexamethasone (DM), or saline (S) before exposure to audiovisual (barking dog) and insulin-induced hypoglycemic stress.
- Experiments were conducted in a controlled manner to exclude confounding effects of prior stress exposure.
Main Results:
- Both stressors elevated ACTH, F, Epi, and NE, with insulin-induced hypoglycemia eliciting a greater response than audiovisual stress.
- Dexamethasone (DM) pretreatment completely blocked ACTH and F responses to stress.
- DM and cortisol attenuated the Epi response to hypoglycemia but not to audiovisual stress. Norepinephrine (NE) responses were unaffected by steroid treatment.
Conclusions:
- Post-stress norepinephrine (NE) release, likely from extra-adrenal sources, is largely independent of steroid hormones.
- The mechanisms governing epinephrine (Epi) release from the adrenal medulla differ between audiovisual and hypoglycemic stress.
- These distinct mechanisms may involve differential central glucocorticoid receptor input to the splanchnic outflow pathways in response to varying stress types.