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Trassanee Chatmethakul Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Robert D Roghair Stead Family Department of Pediatrics, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA

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Consistent with the paradigm shifting observations of David Barker and colleagues that revealed a powerful relationship between decreased weight through 2 years of age and adult disease, intrauterine growth restriction (IUGR) and preterm birth are independent risk factors for the development of subsequent hypertension. Animal models have been indispensable in defining the mechanisms responsible for these associations and the potential targets for therapeutic intervention. Among the modifiable risk factors, micronutrient deficiency, physical immobility, exaggerated stress hormone exposure and deficient trophic hormone production are leading candidates for targeted therapies. With the strong inverse relationship seen between gestational age at delivery and the risk of hypertension in adulthood trumping all other major cardiovascular risk factors, improvements in neonatal care are required. Unfortunately, therapeutic breakthroughs have not kept pace with rapidly improving perinatal survival, and groundbreaking bench-to-bedside studies are urgently needed to mitigate and ultimately prevent the tsunami of prematurity-related adult cardiovascular disease that may be on the horizon. This review highlights our current understanding of the developmental origins of hypertension and draws attention to the importance of increasing the availability of lactation consultants, nutritionists, pharmacists and physical therapists as critical allies in the battle that IUGR or premature infants are waging not just for survival but also for their future cardiometabolic health.

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T. NICOL
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B. VERNON-ROBERTS
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D. C. QUANTOCK
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SUMMARY

(1) The three principal natural oestrogens, oestrone, oestriol and 17β-oestradiol, are strong stimulants of the reticulo-endothelial system (RES).

(2) Testosterone had no effect on the RES when administered alone. Doses of testosterone which inhibited the oestrogenic response of the reproductive tract to oestrone and oestriol also inhibited the stimulant effect of these oestrogens on the RES. In contrast, testosterone markedly potentiated the stimulant effect of 17β-oestradiol on the RES even in doses at which the oestrogenic response is inhibited. These results imply that 17β-oestradiol is the principal oestrogen concerned in the control of RES activity, and provide further proof that the oestrogen molecule has two biological activities, one acting on the RES and the other on the reproductive tract, and that they act independently although contained in the same molecule.

(3) Progesterone is a mild RE stimulant. Doses which inhibited the oestrogenic response of the reproductive tract did not affect oestrogen-produced RE stimulation.

(4) Small doses of cortisone stimulated the RES, but high doses depressed RE activity and oestrogen-produced RE stimulation.

(5) Thyroxine had no effect on the RES when acting alone, but markedly potentiates oestrogen-produced RE stimulation.

(6) The hormones of the anterior lobe of the pituitary are all stimulants of the RES; and, with the exception of growth hormone and follicle stimulating hormone, acted in a synergistic manner with oestrogen.

(7) The hormones of the posterior lobe of the pituitary had no effect on the RES.

(8) The results as a whole indicate that the endocrine system exerts a homeostatic influence on RE function, and that 17β-oestradiol is the principal stimulant of the RES and body defence.

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T. NICOL
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B. VERNON-ROBERTS
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D. C. QUANTOCK
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SUMMARY

(1) Oestrone, oestriol, 17β-oestradiol, ethinyloestradiol, oestradiol monobenzoate, diethylstilboestrol, 4-hydroxy-α,β-diethyldibenzyl (HDB), dienoestrol, hexoestrol, triphenylethylene and tri-p-anisylchloroethylene (TACE) stimulated the reticulo-endothelial system (RES) in intact male and in ovariectomized female mice.

(2) Testosterone propionate inhibited the vaginal smear response to all the above oestrogenic compounds. It also inhibited the RE stimulation produced by oestrone, oestriol, ethinyloestradiol, oestradiol monobenzoate, triphenylethylene and TACE but had no effect on RE stimulation by diethylstilboestrol, HDB, dienoestrol or hexoestrol; it markedly potentiated the stimulant effect of 17β-oestradiol on the RES.

(3) The effect on the RES of oestrogen: androgen interaction does not appear to be dependent on the type of androgen used.

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T. NICOL
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B. VERNON-ROBERTS
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D. C. QUANTOCK
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SUMMARY

(1) Testosterone, progesterone, oestriol, 17α-ethynyl-19-nortestosterone and MER-25 were shown to inhibit the vaginal smear response and the uterine growth response to 17β-oestradiol and diethylstilboestrol.

(2) Testosterone potentiated the stimulant effect of 17β-oestradiol on the reticulo-endothelial system (RES); but had no effect on the RE stimulation produced by diethylstilboestrol.

(3) Progesterone had no effect on RE stimulation produced by 17β-oestradiol or diethylstilboestrol.

(4) Oestriol and 17α-ethynyl-19-nortestosterone had no effect on RE stimulation produced by 17β-oestradiol; but both compounds inhibited the stimulant effect of diethylstilboestrol on the RES.

(5) MER-25 inhibited RE stimulation produced by both 17β-oestradiol and diethylstilboestrol.

(6) The effect of anti-oestrogens on oestrogen-produced RE stimulation was shown to depend on the nature of the stimulating oestrogen used.

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T. NICOL
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B. VERNON-ROBERTS
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D. C. QUANTOCK
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SUMMARY

In intact and orchidectomized animals testosterone had no effect on the reticulo-endothelial system (RES) when administered alone; it potentiated the stimulant effect of 17β-oestradiol on the RES, but had no effect on the RE stimulation produced by diethylstilboestrol. Progesterone was a mild RE stimulant; it had no effect on the RE stimulation produced by 17β-oestradiol or diethylstilboestrol.

Both testosterone and oestrogen caused weight increase in the levator ani of orchidectomized animals; progesterone had no effect. Testosterone and progesterone had no effect on the myotrophic action of 17β-oestradiol, but both compounds inhibited the myotrophic effect of diethylstilboestrol.

The results show that in the male, as in the female, the action of oestrogen on the RES is independent of its action on the reproductive tract, although these two biological activities are contained in the same molecule.

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T. NICOL
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B. VERNON-ROBERTS
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D. C. QUANTOCK
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The present investigation deals with the effects of oestriol, 16-epioestriol, 2-methoxyoestrone and 2-hydroxyoestradiol-17β, when administered alone or together with oestradiol-17β, on the phagocytic activity of the reticulo-endothelial system (RES) and on the reproductive tract in ovariectomized mice. Female mice (T.O. Swiss strain), weighing 20–25 g., were used. Five animals were used to assess the effects of each dose of a compound, or combination of compounds, and ten animals were used as controls. They were treated once daily for 4 days and phagocytic activity was assessed by the carbon clearance method (Nicol, Vernon-Roberts & Quantock, 1965) on the 5th day. The mice were classified as oestrogen-positive or oestrogen-negative depending on the absence or presence of leucocytes in the vaginal smears (Biggers & Claringbold, 1954). Oestradiol-17β was administered orally by stomach tube. Oestriol, 16-epi-oestriol, 2-methoxyoestrone and 2-hydroxyoestradiol-17β were given by s.c. injection, each dose being dissolved in 0·2 ml. arachis oil.

Phagocytic

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Chad D Osterlund Department of Psychology and Neuroscience, University of Colorado, UCB 345, Boulder, Colorado 80309, USA

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Vanessa Thompson Department of Psychology and Neuroscience, University of Colorado, UCB 345, Boulder, Colorado 80309, USA

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Laura Hinds Department of Psychology and Neuroscience, University of Colorado, UCB 345, Boulder, Colorado 80309, USA

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Robert L Spencer Department of Psychology and Neuroscience, University of Colorado, UCB 345, Boulder, Colorado 80309, USA

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Stress-induced activation of hypothalamic paraventricular nucleus (PVN) corticotropin-releasing hormone (CRH) neurons trigger CRH release and synthesis. Recent findings have suggested that this process depends on the intracellular activation (phosphorylation) of ERK1/2 within CRH neurons. We have recently shown that the presence of glucocorticoids constrains stress-stimulated phosphorylation of PVN ERK1/2. In some peripheral cell types, dephosphorylation of ERK has been shown to be promoted by direct glucocorticoid upregulation of the MAP kinase phosphatase 1 (Mkp1) gene. In this study, we tested the hypothesis that glucocorticoids regulate Mkp1 mRNA expression in the neural forebrain (medial prefrontal cortex, mPFC, and PVN) and endocrine tissue (anterior pituitary) by subjecting young adult male Sprague–Dawley rats to various glucocorticoid manipulations with or without acute psychological stress (restraint). Restraint led to a rapid increase in Mkp1 mRNA within the mPFC, PVN, and anterior pituitary, and this increase did not require glucocorticoid activity. In contrast to glucocorticoid upregulation of Mkp1 gene expression in the peripheral tissues, we found that the absence of glucocorticoids (as a result of adrenalectomy) augmented basal mPFC and stress-induced PVN and anterior pituitary Mkp1 gene expression. Taken together, this study indicates that the presence of glucocorticoids may constrain Mkp1 gene expression in the neural forebrain and endocrine tissues. This possible constraint may be an indirect consequence of the inhibitory influence of glucocorticoids on stress-induced activation of ERK1/2, a known upstream positive regulator of Mkp1 gene transcription.

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P. Boulanger
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M. Desaulniers
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G. Bleau
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K. D. Roberts
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A. Chapdelaine
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Sex steroid concentrations in plasma collected from the canine deferential vein were measured, after separation, by radioimmunoassay. The concentrations found were compared with those in the peripheral plasma. The mean concentrations of androstenedione, testosterone, 5α-dihydrotestosterone, 5α-androstane-3α,17β-diol, 5α-androstane-3β,17β-diol and oestradiol-17β were 13·2, 14·7, 8·9, 4·6, 8·0 and 7·5 fold higher respectively in plasma from the deferential vein than in peripheral plasma. A close anatomical relationship was found between the vasa deferentia, the deferential vein and the peripheral plasma as well as between the deferential vein and the prostate gland. These findings emphasize and extend earlier conclusions that high levels of sex steroids present in the deferential vein could have a local influence on the growth of the prostate.

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Laura L Hernandez Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA
Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA

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Sean W Limesand Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA

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Jayne L Collier Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA

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Nelson D Horseman Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA

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Robert J Collier Department of Animal Sciences, Department of Molecular and Cellular Physiology, University of Arizona, Tucson, Arizona 85721, USA

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Recent studies in dairy cows have demonstrated that serotonergic ligands affect milk yield and composition. Correspondingly, serotonin (5-HT) has been demonstrated to be an important local regulator of lactational homeostasis and involution in mouse and human mammary cells. We determined the mRNA expression of bovine 5-HT receptor (HTR) subtypes in bovine mammary tissue (BMT) and used pharmacological agents to evaluate functional activities of 5-HT receptors. The mRNAs for five receptor isoforms (HTR1B, 2A, 2B, 4, and 7) were identified by conventional real-time (RT)-PCR, RT quantitative PCR, and in situ hybridization in BMT. In addition to luminal mammary epithelial cell expression, HTR4 was expressed in myoepithelium, and HTR1B, 2A, and 2B were expressed in small mammary blood vessels. Serotonin suppressed milk protein mRNA expression (α-lactalbumin and β-casein mRNA) in lactogen-treated primary bovine mammary epithelial cell (BMEC) cultures. To probe the functional activities of individual receptors, caspase-3 activity and expression of α-lactalbumin and β-casein were measured. Both SB22489 (1B antagonist) and ritanserin (2A antagonist) increased caspase-3 activity. Expression of α-lactalbumin and β-casein mRNA levels in BMEC were stimulated by low concentrations of SB224289, ritanserin, or pimozide. These results demonstrate that there are multiple 5-HT receptor isoforms in the bovine mammary gland, and point to profound differences between serotonergic systems of the bovine mammary gland and the human and mouse mammary glands. Whereas human and mouse mammary epithelial cells express predominately the protein for the 5-HT7 receptor, cow mammary epithelium expresses multiple receptors that have overlapping, but not identical, functional activities.

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A. C. Roberts
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M. H. Hastings
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N. D. Martensz
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J. Herbert
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ABSTRACT

The role of endogenous opiates in the regulation of photoperiodically induced testicular regression was studied in the male Syrian hamster. In reproductively active hamsters exposed to a long photoperiod (LD; 16 h light: 8 h darkness) or to short days (SD; 8 h light: 16 h darkness) for 20 weeks or to SD after pinealectomy, administration of naloxone, a competitive opiate receptor antagonist, at doses of 2·5–20 mg/kg, significantly increased serum LH concentrations. In marked contrast, these doses of naloxone did not produce any change in LH levels in reproductively quiescent hamsters exposed to SD for 8 weeks.

The influence of gonadal steroids on the LH response to naloxone was studied in hamsters castrated or castrated and implanted s.c with a capsule containing testosterone. Naloxone did not induce LH release in castrated hamsters maintained in LD or in SD, but this response was restored in LD but not SD when serum testosterone concentrations were maintained at levels similar to those observed in intact reproductively active hamsters.

These results show that inhibition of reproduction by the photoperiod prevents naloxone-induced LH release in the male hamster. This lack of response to naloxone is not due, however, to the lower testosterone titres present in these animals compared with reproductively active animals. Responsiveness to naloxone can be restored when the animal is rendered insensitive to the inhibitory photoperiod either by removal of the pineal gland or by induction of photorefractoriness by extended exposure to SD.

J. Endocr. (1985) 106, 243–248

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