Effect of estrogen on calcium and sodium transport by the nephron luminal membranes

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 using the Millipore filtration technique. Incubation of proximal tubules with the hormone did not influence Ca 2+ uptake by the luminal membranes. In contrast, incubation of distal tubules with 10 8 M 17 -estradiol for 30 min decreased the initial uptake of 0·5 mM Ca 2+ from 0·34 0·04 (...) to 0·17 0·04 pmol/µg per 5 s (P<0·05). In the presence of 100 mM Na + , 0·5 mM Ca 2+ uptake was strongly diminished and the effect of 17 -estradiol disappeared (0·17 0·01 and 0·21 0·07 pmol/µg per 5 s in vesicles from the control and treated tubules). Direct incubation of the membranes with 17 -estradiol, however, failed to show any influence of the hormone on Ca 2+ transport. The action of 17 -estradiol was dose-dependent, with a half-maximal effect at approximately 10 9 M. Ca 2+ uptake by the distal tubule membranes presents dual kinetics. 17 -Estradiol decreased the V max value of the high-affinity component from 0·42 0·02 to 0·31 0·03 pmol/µg per 10 s (P<0·02). In contrast with the effect of the hormone on Ca 2+ transport, estradiol increased Na + uptake by both the proximal and distal tubule luminal membranes. In conclusion, incubation of proximal and distal tubules with estrogen decreases Ca 2+ reabsorption by the high-affinity Ca 2+ channels of the distal luminal membranes, and enhances Na + transport by the membranes from proximal and distal nephrons.

Gender-dependent effects of aging on the kidney

“…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.…”

Estrogen modulates ClC-2 chloride channel gene expression in rat kidney

“…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].…”

“…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].…”

17β-Estradiol induces nongenomic effects in renal intercalated cells through G protein-coupled estrogen receptor 1

“…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.…”