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Influence of Arachidonic Acid on the Endocrine Response to Stress (pp.51-62) $100.00
Authors:  (Amy Tse, Andy K. Lee and Frederick W. Tse)
Abstract:
A key component of the endocrine response to stress is the release of corticotrophinreleasing
hormone from the hypothalamus, which in turn stimulates the release of
adrenocorticotropic hormone from the corticotropes in the anterior pituitary gland. A
consequence of the adrenocorticotropic hormone release is the synthesis and secretion of
the stress hormone, cortisol, from the adrenal cortex. High level of cortisol in the body is
linked to many diseases, including obesity, diabetes, hypertension and an impairment in
immune response.
Upon stress, arachidonic acid is generated in pituitary corticotropes. Here, we
described how arachidonic acid activated a specific type of background K+ channels
called TREK-1, in mouse pituitary corticotropes.
The activation of TREK-1 channels caused the membrane potential of corticotropes
to become more negative, thus, opposing the depolarizing action of corticotrophinreleasing
hormone. We suggest that the accumulation of arachidonic acid in pituitary
corticotropes during chronic stress acts as a negative regulator to prevent excessive
adrenocorticotropic hormone secretion. Arachidonic acid also negatively regulates the
downstream target of adrenocorticotropic hormone, the adrenal cortical cells. The
inhibitory actions of arachidonic acid on corticotropes and adrenal cortical cells suggest
that arachidonic acid is a potent inhibitor of stress hormone production and secretion.
This may reflect potential health benefits of arachidonic acid in the prevention and
treatment of stress-related disorders. 


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Influence of Arachidonic Acid on the Endocrine Response to Stress (pp.51-62)