| 1658985 |
Stoker TE, Goldman JM, Cooper RL, McElroy WK: Influence of chlordimeform on alpha-adrenergic receptor-associated mechanisms of hormonal regulation in the rat: pituitary and adrenocortical secretion. Toxicology. 1991;69(3):257-68.
The acaricide chlordimeform (CDF) has been reported to have effects on the central nervous system that appear to involve an interaction with alpha-adrenergic receptor-mediated mechanisms of neurotransmission. The present study examined the effects of CDF on adrenocortical and pituitary prolactin secretion, which are known to involve central adrenergic receptors. Male Long-Evans rats were injected i.p. with 20 or 50 mg/kg CDF and killed after 1, 4, 8 or 24 h. Both noninjected and saline-injected controls were included. Dosing was structured so that trunk blood could be collected during the morning nadir of circulating corticosterone (CORT). Assays for plasma adrenocorticotropic hormone (ACTH), CORT and prolactin (PRL) showed that with 50 mg/kg, all three hormones rose sharply by 1 h. CORT increased in a dose-dependent fashion and declined over the ensuing 8 h. Other rats were treated with the alpha-adrenergic antagonist phenoxybenzamine (PBZ, 20 mg/kg) or the alpha-agonist clonidine (CLON, 0.6 mg/kg) 40 min before and killed 1 h after CDF (25 mg/kg) injection. CLON was found to completely suppress the CDF-induced rise in CORT, while PBZ enhanced the CORT/ACTH response to CDF. CLON also significantly elevated PRL, an alteration not seen in the CLON-pretreated CDF rats. Dexamethasone was able to block the CDF-induced rise in CORT and significantly suppressed PRL levels in both saline- and CDF-treated groups. These effects indicate that CDF is interfering with a regulatory signal mediated by alpha-adrenergic receptor-associated activity. |
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