Abstract:
:Depletion of hypothalamic norepinephrine (NE) and epinephrine by administration of diethyldithiocarbamate abolished the stimulatory effects of intraventricular (IVT) angiotensin II (AII) on LH release in ovariectomized rats pretreated with estradiol and progesterone. The increase in blood LH produced by IVT NE or iv LHRH was unaffected in these drug-treated animals. Selective depletion of hypothalamic epinephrine by the administration of LY134046 (8,9-dichloro-2,3,4,5-tetrahydro-1H-2-benzazepine hydrochloride) potentiated the effect of AII on LH secretion. Blockade of alpha 1-, alpha 2-, or beta-adrenergic receptors resulted in a transient increase in basal LH levels. The stimulation of LH secretion induced by IVT AII or NE was unaffected by alpha 1-receptor blockade with prazosin, but was abolished by alpha 2-receptor blockade with yohimbine. beta-Receptor blockade with propranolol potentiated both NE- and AII-induced LH release. AII receptor blockade with IVT saralasin prevented the LH rise due to AII without modifying that due to NE. Taken together, these data suggest that IVT AII stimulates LH release in ovariectomized rats treated with estradiol and progesterone by releasing endogenous NE, which, in turn, acts on facilitatory alpha 2-receptors to affect LH secretion, presumably by increasing the secretion of LHRH. Exogenous NE also acts at this receptor. beta-Receptors provide inhibitory tone to this facilitatory system, and blockade of this receptor subtype results in potentiated LH responses to both AII and NE.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Steele MK,Ganong WFdoi
10.1210/endo-119-6-2728subject
Has Abstractpub_date
1986-12-01 00:00:00pages
2728-36issue
6eissn
0013-7227issn
1945-7170journal_volume
119pub_type
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