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J Appl Physiol 93: 752-758, 2002. First published February 1, 2002; doi:10.1152/japplphysiol.00425.2001
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Vol. 93, Issue 2, 752-758, August 2002

Rapid effects of 17beta -estradiol and progesterone on sheep visceral and parietal pleurae via a nitric oxide pathway

C. Hatzoglou1,2, K. I. Gourgoulianis3, A. Hatzoglou4, E. Castanas4, and P. A. Molyvdas1

Departments of 1 Physiology and 3 Respiratory Medicine, Medical School, University of Thessaly, and 2 General Hospital of Larissa, 412 22 Larissa; and 4 Department of Laboratory Medicine, Medical School, University of Grete, 71110 Heraklion, Greece


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

We investigated the effects of 17beta -estradiol and progesterone on transepithelial electrical resistance (RTE) in sheep visceral and parietal pleurae. Specimens of intact pleurae from adult female sheep were used. The samples were transferred to the laboratory within 30 min after death of the animal in a Krebs-Ringer solution at 4°C. The pleura was then mounted as a planar sheet in Ussing-type chambers, and electrical measurements were made. There was an increase in RTE in all of the samples examined after addition of 17beta -estradiol and progesterone in visceral and parietal pleurae. This increase was rapid within 1 min, lasted for ~15 min, returned to the basal level within 30-45 min, and was dose dependent. Tamoxifen, an estrogen receptor antagonist, did not significantly eliminate the effect of 17beta -estradiol. Furthermore, no steroid receptors were identified in cytosolic preparations of visceral and parietal pleura with ligand binding assays. The estrogen- and progesterone-induced increase in RTE in both visceral and parietal pleurae was affected by addition of an inhibitor of nitric oxide synthase. Indeed, previous administration of Nomega -nitro-L-arginine methyl ester prevented the increase in RTE by 17beta -estradiol and progesterone. These results suggest that 17beta -estradiol and progesterone induce an increase in RTE in both visceral and parietal pleura and thus alter the transepithelial permeability. The effect of steroids may be accounted for by rapid release of nitric oxide in pleura.

estrogen; permeability; Ussing system


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

PLEURAL EFFUSIONS ARE OBSERVED in some women during pregnancy and in women with ovarian hyperstimulation syndrome (OHSS) and Meigs syndrome. Normal pregnancy could promote transudation of fluid into the pleural space because of increased hydrostatic pressure of systemic circulation, increased blood volume, and decreased colloid osmotic pressure (14). Plasma estrogen concentrations increase dramatically during gestation. High-estrogen states are associated with electrolyte and water transport, resulting in alteration of permeability (15). OHSS is still the major iatrogenic complication of ovarian stimulation with exogenous gonadotropins in cases of primary and secondary infertility. A thoracic hydrothorax is a well-known complication of the severe form (23). The pathogenesis of fluid exudation in OHSS is still obscure. The high-plasma and urinary steroid levels observed in those with this syndrome, coupled with the effect of estrogens in inducing fluid retention and changes in vessel permeability, suggest that steroids play an important role in the pathogenesis (9, 25, 36, 38). Patients with Meigs syndrome have ovarian tumors, usually fibroma, associated with hydrothorax and ascites. The mechanism of formation of peritoneal and pleural effusion is not well documented. The most likely pathogenesis ascribes the fluid formation to the filtration of interstitial fluid in the peritoneal through the tumor capsule and the diffusion to the pleural space through the diaphragm lymphatic vessels at the Bochdalek foramen. Hormonal stimulation is another proposed mechanism (13). An alternative explanation is that the hormonal changes induced by pregnancy, OHSS, and Meigs syndrome causes an alteration in pleura permeability and stimulates pleural effusion.

The purpose of this study was to investigate the effects of 17beta -estradiol and progesterone on transepithelial electrical resistance (RTE) in parietal and visceral sheep pleura. Furthermore, the involvement of the nitric oxide (NO) system was studied. Because of the anatomic differences between the visceral and parietal pleura (24), the measurements of the visceral membrane were compared with those of the parietal membrane.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Intact sheets of visceral and partial pleura were obtained from adult sheep. We used pleura obtained from female, cycling sheep to avoid gender-related differences in the response to estrogen. The samples were collected from a slaughterhouse. The pleurae were kept in oxygenated Krebs-Ringer solution at 4°C and transferred to the laboratory within 30 min after death of the animal. Care was taken to touch the surface as little as possible. Immediately after removal, the pleural tissue was placed in Krebs-Ringer bicarbonate (KRB) solution. The KRB solution was balanced at pH 7.4 and contained (in mM) 117.5 NaCl, 1.15 NaH2PO4, 24.99 NaHCO3, 5.65 KCl, 1.18 MgSO4, 2.52 CaCl2, and 5.55 glucose. The KRB solution was bubbled with 95% O2-5% CO2. If experiments were not immediately performed, the pleurae were stored in KRB solution at 4°C along with segments of the diaphragm and lungs, thus permitting multiple experiments on the tissues of a single animal.

Pieces of visceral pleura were carefully stripped from underlying lung and examined for evidence of holes or adherent lung tissue by visual inspection. The pieces were mainly from the surface of the left and right caudal lobes as well as from the middle and cranial lobes. Parietal pleura was stripped from the diaphragm and examined in a similar way. We studied the effect of stripping the tissue from the lung, the rib cage, and diaphragm. We found the results to be the same as those from mediastinal pleurae that were free standing and required no stripping for tissue bath studies.

The pleura was mounted as a planar sheet separating two reservoirs of fluid in acrylic Ussing-type chambers attached to glass reservoirs. The pleura was mounted between two recessed O rings, and a tight seal was obtained by applying a very small amount of silicone (SYLGAR D Silicone-elastomer kit) along the rim of each O ring. This method of mounting the tissue has been shown to minimize edge effect (21). Each chamber was conical in shape with a total volume (including the reservoir) of 20 ml. The cross-sectional area of the exposed tissue between the reservoirs was 1.43 cm2. The temperature in the chamber was maintained at 37°C, and the KRB solution in each compartment was continuously bubbled with a 95% O2-5% CO2 gas mixture.

The transepithelial potential difference across the visceral and parietal pleura was measured with 3 M KCl 3% agar bridges placed 3 mm on either side of the membrane. These bridges were connected on either side to Ag/AgCl electrodes, and output was amplified (model DVC-3 with input impedance 1012 Omega , Word Precision Instruments). To determine the voltage response to an external current, direct current provided by a voltage-clamp apparatus (model DVC-1000, World Precision Instruments) was passed through the tissue via 3 M KCl agar bridges placed in the reservoirs connected to each hemichamber.

Visceral or parietal pleura was mounted in the chamber, bathed on both sides with KRB solution. A current of variable intensity (range 0-300 µA, -300-0 µA) was then applied, and the voltage response of the visceral and parietal pleura was measured. The RTE was calculated, by using Ohm's law, from the voltage deflections produced in response to constant current pulses across the tissue. Changes in paracellular permeability were determined in terms of changes in RTE.

Before the start of each experiment, the pleura was allowed to equilibrate for at least 30 min to 1 h. In the initial set of experiments, electrical measurements were made on visceral and parietal pleura mounted in the chamber and bathed with KRB solution on both sides (control experiments). The dose response to 17beta -estradiol the was evaluated (concentrations of 17beta -estradiol ranged from 10-9 to 10-5 M). Parallel studies were also performed with progesterone in both pleurae. In some studies, 17beta -estradiol (10-6 M; n = 6) or progesterone (10-6 M; n = 6) were added to the basolateral and apical surface of visceral (n = 6) and parietal (n = 6) pleura. Measurements of RTE were made after exposure to substances for 1 or 6 h. The effects of 17beta -estradiol and progesterone were observed when the hormones were present on both sides of the pleura. Because 17beta -estradiol is lipophilic and readily crosses the membrane, its presence on both sides of the membrane is not unexpected. In a number of cases, the estrogen receptor antagonist tamoxifen (10-6 M; n = 6) or tamoxifen (10-5 M) plus 17beta -estradiol (10-6 M; n = 6) were added to the KRB solution to either the visceral (n = 6) or parietal (n = 6) pleura. Pleural fragments were also stimulated with various concentrations of tamoxifen (10-9 to 10-5 M). Transepithelial potential difference and voltage response to applied current were measured after 1- or 6-h treatments. A series of experiments were conducted to find out whether 17beta -estradiol or progesterone induced NO production. To this end, Nomega -nitro-L-arginine methyl ester (L-NAME) an NO synthase (NOS) inhibitor (10-5 M; n = 6) or L-NAME (10-5 M) plus 17beta -estradiol (10-6 M; n = 6) or progesterone (10-6 M; n = 6) were added to the KRB solution across both the visceral (n = 6) and parietal (n = 6) pleura. Electrical measurements were made for 30 min. All solutions were freshly prepared before each experiment, heated at 37°C, and continuously bubbled with a 95% O2-5% CO2 gas mixture. 17beta -Estradiol, progesterone, and tamoxifen were dissolved in 95% ethanol and added at a dilution that resulted in a final concentration of 0.95% ethanol. This concentration did not affect RTE in any experiment. L-NAME was prepared directly in KRB solution. Each experiment was repeated six times. Each experiment was simultaneously performed with a control from the same tissue source to exclude experimental drift in NO release unrelated to the study drugs. If an antagonist of estrogen or a NOS inhibitor was used, it was administered 2 min before 17beta -estradiol or progesterone.

To investigate the existence of steroid receptors in pleura, tissue fragments of visceral and parietal pleura were pulverized in liquid nitrogen with a dismembrator (Type MM2; Retsch, Rheinland, Germany). The resulting powder was then suspended in Tris buffer (10 mmol/l Tris · HCl, pH 7.4, containing 1.5 mmol/l EDTA, 0.5 mmol/l dithioltreitol, 10 mmol/l sodium molybdate, and 100 ml/l glycerol) and centrifuged for 50 min at 100,000 g. The supernatant was immediately analyzed for steroid receptors according to a previously described ligand binding assay (19). Briefly, the cytosols were incubated at 4°C for 18-20 h with 17beta -[2,4,6,7-3H]estradiol (Amersham) or [6,7-3H]Org-2058 (Amersham) to assay the estrogen receptor and progesterone receptor, respectively. Nonspecific binding was determined by adding to the reaction mixture 10 µmol/l of diethylstilbestrol for the estrogen receptor assay and Org-2058 for the progesterone receptor assay. The radioactivity was counted in a liquid scintillation counter (Tricards 4000; Packard Instruments, Meriden, CT) with 80% efficiency for tritium.

Statistical analysis was performed with SPSS for Windows. Data are presented as means ± SD, and significance of differences between means was estimated by paired t-test. We accepted a P value of <0.05 as being statistically significant.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The effects of steroids on RTE across visceral and parietal pleura were examined. Figure 1 shows that both steroids increase RTE in pleura in a dose-dependent manner. We used concentrations of 17beta -estradiol and progesterone that ranged from 10-9 to 10-5 M and found that RTE increased in both pleurae at concentrations >10-8 M. The maximal effect for visceral pleura was a 43% increase in RTE at 10-5 M for both hormones (Fig. 1A); in the parietal pleura, RTE was increased 43% with 10-5 M 17beta -estradiol and was increased 55% with 10-5 M progesterone (Fig. 1B).


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  		Fig. 1.   Dose-dependent increase in transepithelial electrical resistance (RTE) after administration of 17beta -estradiol and progesterone across visceral (A) and parietal (B) pleura. The changes in RTE were obtained 1 min after drug exposure. The effect of 17beta -estradiol and progesterone was not evident at concentrations below 10-7 M. Values are means ± SD; n = 6 experiments. * P < 0.01 vs. control; ** P < 0.05 vs. control.

Pleurae were also treated with 17beta -estradiol and progesterone at a concentration of 10-6 M for 6 h. Preliminary results showed that 17beta -estradiol and progesterone had a rapid effect on RTE. Further exposure of pleurae to steroids did not result in other changes in RTE compared with control. On the basis of these results, we performed the experiments and statistical analysis of results for a 1-h period. The administration of 10-6 M 17beta -estradiol resulted in an increase in RTE of 17% and 16% for visceral (Fig. 2A) and parietal (Fig. 2B) pleura, respectively. The effect was rapid, occurring within 1 min, lasted for ~15 min, and returned to the basal level within 30-45 min. Similar effects were observed after addition of 10-6 M progesterone in both visceral (Fig. 2A) and parietal (Fig. 2B) pleura.


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  		Fig. 2.   Time-response effects of 17beta -estradiol (10-6 M) and progesterone (10-6 M) on changes in RTE across visceral (A) and parietal (B) pleura. The increase in RTE was rapid within 1 min, lasted for ~15 min, and returned to the basal levels within 30-45 min in both pleurae. Values are means ± SD; n = 6 experiments. * P < 0.01 vs. control; ** P < 0.05 vs. control.

If the conventional estrogen receptor was responsible for the estrogen-induced increase in RTE, the antiestrogens should block this effect. The effect of the antagonist tamoxifen was studied. However, the increase in RTE induced by 17beta -estradiol (10-6 M) was not affected significantly by first exposing the tissue to tamoxifen (10-5 M) in both visceral (Fig. 3A) and parietal (Fig. 3B) pleura. Only a partial inhibition with tamoxifen was noted. Furthermore, exposure to 10-6 M tamoxifen showed similar effects as steroids.


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  		Fig. 3.   Increase in RTE in visceral (A) and parietal (B) pleura as a result of 17beta -estradiol (10-6 M) and tamoxifen (10-6 M) and inhibition of the 17beta -estradiol-induced increase in RTE by tamoxifen (10-5 M; Est+Tam). The changes in RTE were obtained 1 min after addition of the drugs. Tamoxifen is unable to completely inhibit the 17beta -estradiol-induced increase in RTE. Values are means ± SD; n = 6 experiments. * P < 0.01 vs. control; ** P < 0.05 vs. control.

The concentration-response curve of tamoxifen is shown in Fig. 4. The maximal effect in both pleurae was observed at a concentration of 10-5 M. To investigate the presence of steroid receptors (estrogen and progesterone) in sheep pleura, we used a ligand binding assay. Our results did not show any specific binding sites or steroid receptors, neither in visceral nor in parietal pleura under the conditions used (data not shown).


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  		Fig. 4.   Effect of varying concentrations of tamoxifen on RTE across visceral (A) and parietal (B) pleura. Changes in RTE were obtained 1 min after drug exposure. Results are expressed as means ± SD for 6 separate experiments. * P < 0.05.

It has been suggested that steroids can stimulate NO production. To investigate whether the dose response of 17beta -estradiol and progesterone on the rapid increase in RTE in pleura was correlated with NO, we treated pleural tissue with the NOS inhibitor L-NAME. Our results showed that 10-5 M L-NAME blocked the specific effects of steroids in visceral (Fig. 5A) and parietal (Fig. 5B) pleura.


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  		Fig. 5.   Effect of 17beta -estradiol (10-6 M; Estr), progesterone (10-6 M; Prog), Nomega -nitro-L-arginine methyl ester (L-NAME; 10-5 M), and combined effects of 17beta -estradiol plus L-NAME (Est+L-NAME) and progesterone plus L-NAME (Pro+L-NAME) on RTE across visceral (A) and parietal (B) pleura. The changes in RTE were obtained 1 min after administration of the drugs. L-NAME is able to significantly reduce the increase in RTE caused by 17beta -estradiol and progesterone. Values are means ± SD; n = 6 experiments. * P < 0.01 vs. control; ** P < 0.05 vs. 17beta -estradiol; #P < 0.05 vs. progesterone.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The present study demonstrates that 17beta -estradiol and progesterone cause significant changes in the electrical properties of the pleura. They lead to an increase in RTE and thus a decrease in transepithelial permeability in both visceral and parietal pleurae. The effects did not appear to involve the classical intracellular steroid receptors, based on three findings: 1) the effect was rapid, 2) previous administration of the classical estrogen receptor antagonist tamoxifen did not completely inhibit the rapid effects of 17beta -estradiol, and 3) no classical steroid receptors were identified in parietal and visceral pleurae by using ligand binding assays. A role for NO in the estrogen-induced increase in RTE has been suggested because previous administration of the NOS inhibitor L-NAME prevents the increase in RTE.

The effect of 17beta -estradiol was apparent within 1 min; its duration was ~15 min and not affected by previous administration of tamoxifen. Short-term effects that range from milliseconds to a couple of minutes characterize nontranscriptional estrogen actions; these effects are short in both latency and duration in a variety of target tissues. For example, estrogen resulted in rapid action potentials in a pituitary cell line (C1H3/B6) (8), had a short latency effect on neuronal firing rates (7), and resulted in changes in endometrial cell surface morphology (31). Pietras and Szego (28) also reported that 17beta -estradiol rapidly stimulated Ca2+ uptake by endometrial cells. The possible mechanisms for these nonclassical actions are 1) binding to specific steroid hormone receptors present in the cell membrane, 2) binding to and modulation of neurotransmitter membrane receptors such as the GABAA receptor, 3) direct action via classical intracellular receptors, 4) changes in membrane fluidity, and 5) direct activation of second-messenger systems (1, 11, 35).

These diverse modes of action could explain the hormone effects, which may be rapid and have a short or prolonged duration, to address the physiological needs of the individual. The effect of progesterone was similar to that of 17beta -estradiol in RTE, in both visceral and parietal pleura. Nonclassical effects are shown in several cell types. Ke and Ramirez (18) showed that progesterone is capable of rapid release of luteinizing hormone-releasing hormone from the hypothalamus in vitro. Progesterone and its metabolites have also been demonstrated to be potent inhibitors of uterine smooth muscle contractility (30).

The inability of tamoxifen to completely reverse the effect of estrogen and the absence of steroid receptors on sheep pleurae suggest the involvement of nonclassical steroid or other receptor systems. Cross talk between different membrane receptors was previously described in several tissues (16). On the other hand, the possible involvement of the classical steroid receptor in mediating the rapid increase in RTE could not be excluded because tamoxifen has a partial antagonist effect on RTE.

Tamoxifen itself induces an increase in RTE in both visceral and parietal pleura. This increase was rapid, with the same duration but smaller than that induced by steroids. It was found that tamoxifen also blocks cell growth of hormone-unresponsive breast cancer cells, which do not express estrogen receptors. In addition, tamoxifen was shown to be effective for a number of estrogen receptor-negative tumors, including lung cancer, brain cancer, and melanoma (20). Furthermore, tamoxifen has a rapid and substantial inhibitory effect on action potential firing and Ca2+ currents in the clonal pituitary cell line CH3/B6 (34). This indicates that tamoxifen, besides its action as an antiestrogen, has effects on other critical components of intracellular signaling pathways (33). However, the molecular mechanism of such estrogen receptor-independent action is presently unknown. Tamoxifen also exhibits partial antagonist activity. Thus tamoxifen exhibits both partial antagonist and weak agonist effects in the same tissue. Similar results were observed by Castro-Rivera and Safe (3) in HEC1A endometrial adenocarcinoma cells.

Estrogens decrease the transepithelial permeability of pleura by increasing the RTE. The mechanisms by which estrogen increases RTE are not clear. One possible mechanism is that estrogen induced acute changes in the cell size of pleura and thus these changes in cell size affect the RTE. Rapid changes in cell size can be the result of two main mechanisms: acute water shifts, which are usually secondary to acute changes in Na+ or Cl- transport, or rearrangement of cytoskeletal proteins. Other possible mechanisms by which estrogens can modulate the size of pleura cells are changes in membrane permeability (40), modulation of transcellular movement of water (2), and regulation of ion transport mechanisms such as the Na+-K+-ATPase (5), K+ (29), and Ca2+ channels (37). NO was found to inhibit both amiloride-sensitive cation channels and Na+-K+-ATPase and to decrease vectorial Na+ transport across alveolar type II monolayers (22) as well as across cultured distal lung epithelial cells (6). Thus NO may alter the transepithelial permeability with one or more of the above mechanisms. The biochemical steps by which 17beta -estradiol and progesterone increase RTE in visceral (17) and parietal pleura remain unclear, and more work is needed to solve this problem. However, it seems that NO stimulation may present one way by which the rapid effect, by alteration of the membrane permeability of these hormones, is mediated.

Endothelial cells are targets for the actions of the female hormones estrogen and progesterone. In endothelia, some of the effects of estrogen are mediated by the NO system. NO can modulate the permeability of epithelial and endothelial tissues, but there is considerable controversy concerning the role of NO as a mediator of permeability. The dose-response effect of 17beta -estradiol and progesterone on the decrease in permeability correlated with the effect of hormones on the increase in NO. This correlation suggests that NO mediates the decrease in permeability. Studies on the effect of NO on permeability are not entirely in agreement. NO was found to decrease the permeability in human umbilical and pulmonary artery endothelial cell monolayers (39) as well as in the coronary circulation of the rat (12), but it was found to increase the permeability in human umbilical vein endothelial cells (4). In agreement with results previously reported by others (27, 32), L-NAME in the present study failed to completely prevent increases in RTE. One possible explanation for a lack of complete inhibition could have been that the concentration of L-NAME used in this study was not sufficient to inhibit all NOS. Alternatively, NO may act in association with other relaxing factors or hyperpolarizing factors or may alter the response of the tissue to these substances (10, 26).

The influence of hormones on the electrical properties of a membrane is of great importance to the changes in the functioning of a cell. A constant hormonal background or changes in it, in various situations, acting on membrane processes, in many respects will determine the basal level of the permeability of cells and these changes will result in various influences on the organism. The increase in RTE required high concentrations of 17beta -estradiol and progesterone, at supraphysiological levels for women. Free estrogens usually do not reach these high levels in the plasma. However, in certain conditions, tissues may be exposed to high levels of steroids. The specific, high level of 17beta -estradiol and progesterone that was studied is readily achieved during pregnancy (15) as well as during OHSS (25). Furthermore, the hormonal stimulation was involved in the pathogenesis of Meigs syndrome (13). During these three situations, permeability of the membranes was shown to be altered and steroids may play an important role in this. Because changes in RTE reflect the passage of ions and thus water, it is possible that the decrease in permeability induced by steroids leads to an increased fluid accumulation and thus prevents the transport of fluid out of the pleural space.

In conclusion, our results show that the sheep visceral and parietal pleurae exhibit an increase in NO after treatment with steroid hormones. The effect of 17beta -estradiol and progesterone is rapid and partially inhibited by tamoxifen. This increase may play an important role in alteration of epithelial permeability in situations like pregnancy, OHSS, and Meigs syndrome.


    ACKNOWLEDGEMENTS

We thank I. Makadasis for technical assistance. We also thank S. Effremidou and E. Souloukou for secretarial assistance in preparation of the manuscript.


    FOOTNOTES

Address for reprint requests and other correspondence: K. I. Gourgoulianis, Medical School, Univ. of Thessaly, 22 Papakyriazi, 412 22 Larissa, Greece (E-mail: kgourg{at}med.uth.gr).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

February 1, 2002;10.1152/japplphysiol.00425.2001

Received 3 May 2001; accepted in final form 8 October 2001.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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