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Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
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Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
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Introduction Pregnancy is a time of dramatic vascular adaptation. Through initial angiogenesis and then sustained vasodilation, the pregnant uterus achieves the biggest drop in vascular resistance of any organ system. This in turn promotes a
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Severance Biomedical Research Institute, Department of Internal Medicine, Yonsei University College of Medicine, 50 Yonsei‐ro, Seodaemun‐gu, Seoul 120-752, Korea
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Introduction All known organisms have the capability to maintain homeostasis in response to environmental challenges. The ability to modify gene expression is a fundamental organismal mechanism of adaptation to environmental stimuli. In particular
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. Physiologic and anatomic adaptation of vasculature to pregnancy Implantation and early vascular remodeling Although it could certainly be argued that hormonal changes associated with the menstrual cycle prepare the uterus for any impending pregnancy
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confer to the latter, a relatively stronger adaptation profile that appears to be related to the ability to regulate NO production ( Rodríguez et al. 2015 ). Considering that thyroid status alterations are one of the major endocrine diseases in
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Introduction Maternal physiological adaptations are central to pregnancy success, balancing fetal and placental demands with the maintenance of maternal homeostasis. Among these maternal adaptations, enhanced activity of the hypothalamic
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ABSTRACT
The influence of adrenalectomy and administration of aldosterone on potassium secretion by colonic epithelium was studied in vivo in rats, particularly in relation to potassium adaptation (induced by feeding a potassium-rich diet) and the response to acute i.v. administration of a potassium load. Adrenalectomy (rats maintained on dexamethasone and saline) impaired the development of potassium adaptation or considerably reduced it if the rats had been previously adapted. The partial adaptation observed in the adrenalectomized rats may be related to the increased plasma potassium concentration developed when these rats received the potassium-rich diet.
Within 2 h of acute aldosterone administration, the response of the potassium secretion rate to acute potassium loading in adrenalectomized rats was significantly improved. When aldosterone (2 μg/day per 100 g body weight, given by osmotic minipump) was added to the replacement treatment, the plasma concentration of potassium was similar to that of the intact rats, and both potassium adaptation and the response to the acute potassium load were completely restored. Transepithelial potential difference and sodium transport were not stimulated, being similar to the values in intact rats. Considerable changes in potassium secretion induced by acute potassium loading did not significantly affect sodium transport.
The findings suggest that the sodium and potassium epithelial pathways are, to a large extent, independently influenced by aldosterone. Aldosterone appears to be essential for complete adaptation and, in a relatively low dose, can completely restore potassium adaptation and the response to acute potassium loads in adrenalectomized rats.
J. Endocr. (1988) 117, 379–386
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). To understand the underlying mechanisms of stress adaptation and related disorders is of high clinical interest. Stress in humans mainly occurs as a consequence of personal interactions or due to a fear of social state loss, for example because of
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of β-cell adaptations in rodent pregnancy ( Rieck & Kaestner 2010 ). Similarly, in human pregnancy, levels of CRH in the peripheral circulation increase as gestation progresses ( Campbell et al . 1987 , Sasaki et al . 1987 ) and CRH
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adaptation syndrome (GAS) ‘the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed and represent rather a response to damage as such.’ The main features of the syndrome were a fall of body
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adaptive growth induced by refeeding ( Shin et al . 2005 , Bahrami et al . 2010 ) or by resection in rodents ( Dahly et al . 2003 ). Exogenous GLP2 enhances intestinal adaptation after major small bowel resection in the rat ( Scott et al . 1998 ) and
