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SUMMARY
The serum concentration of gonadotrophin during several stages of pregnancy was determined in seven mares bred to a stallion and in four mares bred to a jack. To eliminate individual differences, two mares were bred successively to a stallion and to a jack. When the mare is carrying a mule foetus the hormone concentration is approximately one-tenth that associated with a horse foetus. One mare carrying a mule foetus was killed on the 69th day of pregnancy. Though the endometrial cups appeared normal histologically, the endometrial cup secretion was scanty and low in potency. The amount of hormone in the cups themselves was also low.
The genotype of the foetus, we conclude, influences the secretory activity of the endometrial cups.
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Tenovus Institute for Cancer Research, and *Department of Medicine, Welsh National School of Medicine, The Heath, Cardiff, CF4 4XX
(Received 17 April 1974)
Synthetic luteinizing hormone releasing hormone (LH-RH) provides a useful tool for the study of pituitary regulation in the hypothalamo-adenohypophysialgonadal system. Negro-Villar, Orias & McCann (1973) showed that oestradiol-17β given 2 h before injection of LH-RH to ovariectomized rats reduced luteinizing hormone (LH) release. In male dogs, Jones & Boyns (1974) have found that oestradiol-17β or diethylstilboestrol similarly reduces LH release in response to LH-RH given 2·5 h, but not 24 h later. Androgens were without effect in that study.
We now report the gonadotrophin responses to LH-RH in healthy men 2 h after i.m. injection of either oestradiol benzoate (2 mg in 1 ml ethyl oleate), testosterone propionate (5 mg in 1 ml ethyl oleate), or with no acute steroid pretreatment.
Five men volunteered for these ambulatory
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Murdoch, Western Australia, Australia
Department of General Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
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Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Royal College of Surgeons in Ireland, Dublin, Ireland
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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MR activation in macrophages is critical for the development of cardiac inflammation and fibrosis. We previously showed that MR activation modifies macrophage pro-inflammatory signalling, changing the cardiac tissue response to injury via both direct gene transcription and JNK/AP-1 second messenger pathways. In contrast, MR-mediated renal electrolyte homeostasis is critically determined by DNA-binding-dependent processes. Hence, ascertaining the relative contribution of MR actions via DNA binding or alternative pathways on macrophage behaviour and cardiac inflammation may provide therapeutic opportunities which separate the cardioprotective effects of MR antagonists from their undesirable renal potassium-conserving effects. We developed new macrophage cell lines either lacking MR or harbouring a mutant MR incapable of DNA binding. Western blot analysis demonstrated that MR DNA binding is required for lipopolysaccharide (LPS), but not phorbol 12-myristate-13-acetate (PMA), induction of the MAPK/pJNK pathway in macrophages. Quantitative RTPCR for pro-inflammatory and pro-fibrotic targets revealed subsets of LPS- and PMA-induced genes that were either enhanced or repressed by the MR via actions that do not always require direct MR-DNA binding. Analysis of the MR target gene and profibrotic factor MMP12 identified promoter elements that are regulated by combined MR/MAPK/JNK signalling. Evaluation of cardiac tissue responses to an 8-day DOC/salt challenge in mice selectively lacking MR DNA-binding in macrophages demonstrated levels of inflammatory markers equivalent to WT, indicating non-DNA binding-dependent MR signalling in macrophages is sufficient for DOC/salt-induced tissue inflammation. Our data demonstrate that the MR regulates a macrophage pro-inflammatory phenotype and cardiac tissue inflammation, partially via pathways that do not require DNA binding.
