1988
DOI: 10.1016/0143-4179(88)90049-2
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Evidence that long-term administration of a methionine-enkephalin analogue stimulates the growth and steroidogenic capacity of rat inner adrenocortical cells

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Cited by 11 publications
(2 citation statements)
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“…Studies of the effects of enkephalins on adrenal steroidogenesis have mostly used an analogue of met-enkephalin, D-ala2-met-enkephalinamide (DALA). Long-term administration of this peptide has been shown to stimulate the growth and steroidogenic capacity of both zona glomerulosa and zonae fasciculata/reticularis of intact rats treated with dexamethasone and captopril, to inhibit both the secretion of ACTH and the renin-angiotensin system (99)(100)(101). Short term administration of DALA to these dexamethasone treated animals had no effect on corticosterone secretion (99), and this is in agreement with an earlier study ( 102).…”
Section: Evidence For Neural Regulation Of Adrenocortical Functionsupporting
confidence: 88%
“…Studies of the effects of enkephalins on adrenal steroidogenesis have mostly used an analogue of met-enkephalin, D-ala2-met-enkephalinamide (DALA). Long-term administration of this peptide has been shown to stimulate the growth and steroidogenic capacity of both zona glomerulosa and zonae fasciculata/reticularis of intact rats treated with dexamethasone and captopril, to inhibit both the secretion of ACTH and the renin-angiotensin system (99)(100)(101). Short term administration of DALA to these dexamethasone treated animals had no effect on corticosterone secretion (99), and this is in agreement with an earlier study ( 102).…”
Section: Evidence For Neural Regulation Of Adrenocortical Functionsupporting
confidence: 88%
“…There are several alternative hypotheses to explain such a discrep ancy: (i) strain-dependent changes in adrenal responsive ness to circulating ACTH [37] or in corticosterone metab olism: (ii) the existence of ACTH-independent mecha nisms involved in the control of adrenocortical secretion [56.57], Among the latter one could consider: (a) splanch nic innervation of the adrenal, which enhances blood flow to the adrenal cortex and the sensitivity to ACTH [58,59] and involves local release of CRF and other neuropep tides [60,61]; (b) the role of several peptides, including those derived from pro-opiomelanocortin, which are re leased into the blood during stress and are able to increase the adrenocortical response to circulating ACTH [62][63][64], Focusing on LEW rats, the results suggest that the blunted B response to chronic IMO observed in LEW rats is not apparently caused by a defect in basal serum ACTH or in basal PVN CRF biosynthesis. Although it has been shown that the hyporesponsiveness of LEW rats to acute stress is secondary to a defect in hypothalamic CRF bio synthesis and secretion [43,65], it should be taken into account that: (i) the effects of chronic stress on basal CRF mRNA are not comparable to those induced by acute stress; (ii) changes in mRNA cannot be assumed to be always a reflection of peptide activity/secretion since posttranscriptional mechanisms and particularly peptide release might be differentially affected; (iii) in vitro basal hypothalamic arginine vasopressin release is higher in LEW than in FIS rats and this might, at least partially, compensate for the insufficient CRF secretion [66].…”
Section: Discussionmentioning
confidence: 99%