Estrogen to Progesterone Ratio and Fluid Regulatory Responses to Varying Degrees and Methods of Dehydration

The purpose of this study was to investigate the relationship between volume regulatory biomarkers and the estrogen to progesterone ratio (E:P) prior to and following varying methods and degrees of dehydration. Ten women (20 ± 1 year, 56.98 ± 7.25 kg, 164 ± 6 cm, 39.59 ± 2.96 mL•kg•min−1) completed four intermittent exercise trials (1.5 h, 33.8 ± 1.3°C, 49.5 ± 4.3% relative humidity). Testing took place in two hydration conditions, dehydrated via 24-h fluid restriction (Dehy, USG > 1.020) and euhydrated (Euhy, USG ≤ 1.020), and in two phases of the menstrual cycle, the late follicular phase (days 10–13) and midluteal phase (days 18–22). Change in body mass (%BMΔ), serum copeptin concentration, and plasma osmolality (Posm) were assessed before and after both dehydration stimuli (24-h fluid restriction and exercise heat stress). Serum estrogen and progesterone were analyzed pre-exercise only. Estrogen concentration did not differ between phases or hydration conditions. Progesterone was significantly elevated in luteal compared to follicular in both hydration conditions (Dehy—follicular: 1.156 ± 0.31, luteal: 5.190 ± 1.56 ng•mL−1, P < 0.05; Euhy—follicular: 0.915 ± 0.18, luteal: 4.498 ± 1.38 ng·mL−1, P < 0.05). As expected, E:P was significantly greater in the follicular phase compared to luteal in both hydration conditions (Dehy—F:138.94 ± 89.59, L: 64.22 ± 84.55, P < 0.01; Euhy—F:158.13 ± 70.15, L: 50.98 ± 39.69, P < 0.01, [all •103]). Copeptin concentration was increased following 24-h fluid restriction and exercise heat stress (mean change: 18 ± 9.4, P < 0.01). We observed a possible relationship of lower E:P and higher copeptin concentration following 24-h fluid restriction (r = −0.35, P = 0.054). While these results did not reach the level of statistical significance, these data suggest that the differing E:P ratio may alter fluid volume regulation during low levels of dehydration but have no apparent impact after dehydrating exercise in the heat.

Interplay between renal endothelin and purinergic signaling systems

Alterations in extracellular fluid volume regulation and sodium balance may result in the development and maintenance of salt-dependent hypertension, a major risk factor for cardiovascular disease. Numerous pathways contribute to the regulation of sodium excretion and blood pressure, including endothelin and purinergic signaling. Increasing evidence suggests a link between purinergic receptor activation and endothelin production within the renal collecting duct as a means of promoting natriuresis. A better understanding of the relationship between these two systems, especially in regard to sodium homeostasis, will fill a significant knowledge gap and may provide novel antihypertensive treatment options. Therefore, this review focuses on the cross talk between endothelin and purinergic signaling as it relates to the renal regulation of sodium and blood pressure homeostasis.

Serum and glucocorticoid regulated kinase and disturbed renal sodium transport in diabetes

Diabetes is associated with a number of side effects including retinopathy, neuropathy, nephropathy and hypertension. Recent evidence has shown that serum and glucocorticoid regulated kinase-1 (SGK1) is increased in models of diabetic nephropathy. While clearly identified as glucocorticoid responsive, SGK1 has also been shown to be acutely regulated by a variety of other factors. These include insulin, hypertonicity, glucose, increased intracellular calcium and transforming growth factor-β, all of which have been shown to be increased in type II diabetes. The principal role of SGK1 is to mediate sodium reabsorption via its actions on the epithelial sodium channel (now known as sodium channel, nonvoltage-gated 1). Small alterations in the sodium resorptive capacity of the renal epithelia may have dramatic consequences for fluid volume regulation, and SGK1 maybe responsible for the development of hypertension associated with diabetes. This short commentary considers the evidence that supports the involvement of SGK1 in diabetic hypertension, but also discusses how aberrant sodium reabsorption may account for the cellular changes seen in the nephron.

IZMENENIYa KOSTNOY TKANI ChELOVEKAV KOSMIChESKOM POLETE: O VOZMOZhNYKh MEKhANIZMAKh OSTEOPENII

Some results of possible participation of bone metabolism regulation different levels in the bone changes caused by microgravity are presented taking into account the body fluid redistribution which usually accompany the space flight. The primary starting changes associate with biomechanical factors and realize on the strictly bone level (osteocytic osteolysis, breach of «collagen-crystal» connection, slowing of osteoblastic histogenesis). There are calcium homeostasis distortion on the extrabone (tissue, organs) level: decrease of calcium intestinal absorption and renal reabsorption. Changes in the hierarchy of ion and fluid volume regulation systems may provoke the osteoclastic resorption, which intensify the bone loss.