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Hypoglycaemia‐Induced Inhibition of Pulsatile Luteinizing Hormone Secretion in Female Rats: Role of Oestradiol, EndogenousOpioids and the Adrenal Medulla
Author(s) -
Cagampang Felino Ramon A.,
Cates Philippa S.,
Sandhu Satwinder,
Strutton Paul H.,
McGarvey Cliona,
Coen Clive W.,
O’Byrne Kevin T.
Publication year - 1997
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1997.00653.x
Subject(s) - medicine , endocrinology , ovariectomized rat , pulsatile flow , adrenal medulla , luteinizing hormone , medulla , opioid peptide , hormone , opioid , catecholamine , receptor
Oestradiol (E 2 ) has been shown to exacerbate the inhibitory effect of hypoglycaemic stress on gonadotrophin‐releasing hormone pulse generator (GnRH) activity in primates. The mechanism by which this is mediated is not yet known. We therefore aimed to establish whether there is a sensitizing influence of E 2 on the suppression of LH pulsatility in response to hypoglycaemia in the female rat, thus providing a more amenable model in which to study this phenomenon. In ovariectomized Wistar rats with E 2 replacement, insulin‐induced hypoglycaemia (0.5 U/kg iv) resulted in an interruption of pulsatile LH secretion. Induction of the same degree of hypoglycaemia in ovariectomized rats without E 2 replacement was without effect on LH pulsatility. Naloxone administration prevented the hypoglycaemia‐induced inhibition of LH pulses. Because hypoglycaemia is a potent activator of the sympathetic nervous system, we also tested the hypothesis that the adrenal medulla is involved in this suppression of LH pulses in the rat. Adrenomedullectomy completely prevented this inhibitory response to hypoglycaemic stress. These data are consistent with the hypothesis that E 2 sensitizes the GnRH pulse generator to the inhibitory influences of hypoglycaemic stress in the rat. Furthermore, a clear role for both endogenous opioid peptides and the adrenal medulla in the stress‐induced suppression of LH pulsatility is identified.