Abstract:Estrogens are widely used for contraception and osteoporosis prevention. The aim of the present study was to investigate the effect of 17 -estradiol on calcium (Ca 2+ ) transport by the nephron luminal membranes, independently of any other Ca 2+ -regulating hormones. Proximal and distal tubules of rabbit kidneys were incubated with 17 -estradiol or the carrier for various periods of time, and the luminal membranes of these tubules were purified and vesiculated. Ca 2+ uptake by membrane vesicles was measured us… Show more
“…In animal models, estradiol increases sodium uptake through the luminal membranes of both proximal and distal tubules and the presence of estrogen receptors has been confirmed at both sites (52). The role of estrogen in renal salt handling was also demonstrated by Chappell et al (53) using female mRen(2) Lewis strain rats.…”
Section: Changes In Sodium and Water Handlingmentioning
“…In animal models, estradiol increases sodium uptake through the luminal membranes of both proximal and distal tubules and the presence of estrogen receptors has been confirmed at both sites (52). The role of estrogen in renal salt handling was also demonstrated by Chappell et al (53) using female mRen(2) Lewis strain rats.…”
Section: Changes In Sodium and Water Handlingmentioning
“…Those findings were documented in experiments performed on women taking oral contraceptives, as well as in rats, dogs and rabbits treated with estrogen [17,36]. This phenomenon is associated with an increase in renal reabsorption of sodium and chloride from both proximal and distal nephrons; however, the exact mechanisms involved have not yet been identified [4]. Additional evidence for the involvement of sex hormones in renal fluid balance comes from the observation that occurs an expansion of maternal ECFV associated with an increase in renal reabsorption of water, sodium and chloride mainly in pregnant rats between 5-12 days after mating, the period when the plasma levels of estrogen are increased [2].…”
Section: Introductionmentioning
confidence: 95%
“…It is well known that estrogen administration can lead to significant body fluid retention [17,18] and in very high doses it can cause hypertension [23,40]. Several investigators have shown that estrogen is associated with a decrease in urinary excretion of sodium and chloride leading to water body retention and a consequent increase in body weight [4,23,32,40]. Those findings were documented in experiments performed on women taking oral contraceptives, as well as in rats, dogs and rabbits treated with estrogen [17,36].…”
ClC-2 is a CLC family member of chloride channels sensitive to changes in cell volume, pH and voltage. The ClC-2 is widely distributed along the nephron although in the kidney its role still not well understood. Aldosterone studies suggest that ClC-2 expression in the kidney may be hormonally regulated. To explore the possibility that estrogen control ClC-2 expression, we investigated whether its expression changed in the kidney of female Wistar rats subjected to ovariectomy with or without near-physiological or high doses of 17beta-estradiol benzoate treatment for 10 days. Total RNA isolated from rat kidney and dissected nephron segments was analyzed by ribonuclease protection assay and/or a semi-quantitative RT-PCR. The renal ClC-2 protein expression was analyzed by Western blot. The decreased renal expression of ClC-2 mRNA and protein observed in ovariectomized rats was restored to control levels after treatment with low doses of estradiol. Higher dose estradiol lead to an even greater increase in ClC-2 mRNA and protein expression. This change in overall expression was shown to be caused by the modulation of ClC-2 mRNA expression in the proximal tubule. These results suggest that ClC-2 may be involved in estrogen-induced Cl(-) transport in rat kidney.
“…For example, E2 is a crucial player in the prevention of female bone decalcification resulting in osteoporosis (1), and the reduced circulating E2 level is known to be associated with an increased risk of renal stone formation in women after menopause (24). Furthermore, E2-induced fluid retention is caused partly by increased renal tubular Na ϩ reabsorption (8), and P4 has natriuretic actions by directly antagonizing aldosterone at the level of the mineralocorticoid receptors (37). In addition to long-term effects, many steroid hormones exert nongenomic effects either via their classic receptors or through membrane-associated receptors (reviewed in Ref.…”
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