Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Influence of chlordimeform on alpha-adrenergic receptor-associated mechanisms of hormonal regulation in the rat: pituitary and adrenocortical secretion. 165 85

The purpose of this work was to assess whether the non-steroidal anti-inflammatory drugs (NSAIDs) phenylbutazone and ketoprofen, and an adrenocorticotropic hormone (ACTH) induced cortisol surge, reduce the cortisol response which occurs when the local anaesthetic wears off in calves following dehorning. There were four control groups and one dehorned group; also four groups were given local anaesthetic lasting 5h and were dehorned without or with phenylbutazone, ketoprofen or an ACTH injection, one group was injected with ACTH twice (at 0 and 6h) and another received ACTH and 6h later was dehorned. Blood samples were taken before and after dehorning and plasma cortisol concentrations were determined by radio-immunoassay. Dehorning increased the mean plasma cortisol concentrations [max 137 (11)nmoll(-1)] above control values [38 (5)nmoll(-1)] for about 7h, whereas local anaesthesia maintained concentrations at control values until about 5h after dehorning, and then they became elevated until about 10h. The maximum rise in mean concentration which occurred when the local anaesthetic wore off [128 (32)nmoll(-1)] was not affected when phenylbutazone was given before dehorning [141 (28)nmoll(-1)], but was reduced significantly when ketoprofen [65 (17)nmoll(-1)] or ACTH [61 (19)nmoll(-1)] were injected before or at the time of dehorning, respectively. Marked cortisol responses to ACTH injected at 0 and 6h were similar, but the early part of the cortisol response to dehorning 6h after an ACTH injection was reduced. It is suggested that the delayed cortisol response, which began 5h after dehorning, arose both from ketoprofen-sensitive and cortisol-sensitive sensory input as well as from other factors. Phenylbutazone did not affect the sensory input from the amputation wounds in the present calves.
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PMID:Cortisol responses to dehorning of calves given a 5-h local anaesthetic regimen plus phenylbutazone, ketoprofen, or adrenocorticotropic hormone prior to dehorning. 1220 28