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Endocrinology Vol. 138, No. 10 4358-4363
Copyright © 1997 by The Endocrine Society

ARTICLES

Effect of Endothelin-1 on Corticosteroid Secretion by the Frog Adrenal Gland Is Mediated by an EndothelinA Receptor1

Franck Cartier, Isabelle Remy-Jouet, Alain Fournier, Hubert Vaudry2 and Catherine Delarue

European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, Institut National de la Santé et de la Recherche Médicale (INSERM U413), Unité Affiliée au Centre National de la Recherche Scientifique (UA CNRS), University of Rouen (F.C., I.R.J., H.V., C.D.), 76821 Mont-Saint-Aignan, France; and Institut National de la Recherche Scientifique-Santé (INRS-Santé), University of Québec (A.F.), Pointe-Claire, Québec, Canada H9R 1G6

Address all correspondence and requests for reprints to: Hubert Vaudry, European Institute for Peptide Research (IFRMP 23), Laboratory of Cellular and Molecular Neuroendocrinology, INSERM U413, UA CNRS, University of Rouen, 76821 Mont-Saint-Aignan, France. E-mail: hubert.vaudry{at}univ-rouen.fr


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
We have previously reported that endothelin-1 (ET-1) stimulates the in vitro secretion of corticosterone and aldosterone from the adrenal gland of the frog Rana ridibunda. The aim of the present study was to investigate the pharmacological profile of the endothelin receptor subtype involved in the corticotropic effect of ET-1. The mixed ETA/ETB receptor antagonist Ro 47–0203 (10-5 M) totally blocked the stimulatory effect of ET-1 (5 x 10-9 M) on corticosterone and aldosterone secretion. The action of ET-1 was also inhibited by the selective ETA receptor antagonist BQ-485 (10-7 M). In contrast, the selective ETB receptor antagonist IRL 1038 (10-6 M) did not affect the response of the frog adrenal gland to ET-1. In addition, the selective ETB receptor agonist IRL 1620 (10-6 M) did not mimic the stimulatory effect of ET-1. The high affinity ETC receptor agonist endothelin-3 (ET-3) stimulated corticosteroid secretion, but was 400 times less potent than ET-1. Moreover, the action of ET-3 was also blocked by BQ-485 (10-7 M). These data indicate that the stimulatory effects of ET-1 and ET-3 on corticosteroid secretion by the frog adrenal gland are mediated by an ETA receptor subtype.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
THE TERM endothelins (ETs) designates a family of peptides initially isolated from cultured endothelial cells on the basis of their vasoconstrictor activity (1). Analysis of human genomic DNA has revealed the existence of three distinct genes encoding for three endothelin isoforms named ET-1, ET-2, and ET-3 (2). All three ETs comprise 21 amino acids including four cysteine residues. The intramolecular disulfide bridges (Cys1-Cys15 and Cys3-Cys11), as well as the C-terminal tryptophan residue, play a crucial role for the vasoconstrictor activity of endothelins (3, 4).

The effects of endothelins are mediated by at least three types of G-protein-coupled membrane receptors, which exhibit different affinities for the isopeptides (5). The ETA receptor type, which mediates vasoconstriction, exhibits a higher affinity for ET-1 and ET-2 than for ET-3 (6). The ETB receptor does not discriminate between the three isoforms (7); two subtypes of ETB receptors have been identified, one (ETB1) that mediates vasodilation and the other one (ETB2) that elicits constriction (8, 9, 10, 11). The ETC receptor type, which has been cloned from Xenopus laevis dermal melanophores, exhibits high affinity for ET-3 (12) but the physiological significance of this receptor remains unknown.

Besides their well-established vascular effects, ETs display a large array of biological activities (13). In particular, ETs modulate the activity of various endocrine glands, including the pituitary, parathyroid, adrenal medulla, and adrenal cortex (14). We have previously shown that ET-1 is a potent stimulator of corticosterone and aldosterone secretion from the frog adrenal gland (15, 16). The aim of the present study was to determine the type of receptor involved in the corticotropic action of ET-1.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Materials
Synthetic ET-1 was synthetized by the solid-phase methodology as previously described (17). Synthetic ET-3 (human and rat sequence) was purchased from Sigma (St. Louis, MO). Bosentan or Ro 47–0203 (4-tert-butyl-N-[6-(2-hydroxy-ethoxy)-5-(2-methoxy-phenoxy)-2,2'-bipyrimidin-4-yl]-benzene-sulfonamide) was a kind gift from Hoffmann-La Roche (Basel, Switzerland). BQ-485 (perhydroazepin-1-yl-L-leucyl-D-tryptophanyl-D-tryptophan) was generously provided by Banyu Pharmaceuticals (Tsukuba, Japan). IRL 1038 [Cys11-Cys15]ET-1(11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21) and IRL 1620 [N-suc-[Glu9,Ala11,15]ET-1(8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21)] were purchased from Peninsula Laboratories (Merseyside, UK). [1,2,6,7-3H]Corticosterone and [1,2,6,7-3H]aldosterone were purchased from Amersham International (Les Ulis, France). Synthetic human ACTH(1–39) was a generous gift from Ciba-Geigy Laboratories (Basel, Switzerland).

Perifusion experiments
Adult male frogs (Rana ridibunda) originating from Albania were obtained from a commercial source (Couétard, Saint-Hilaire de Riez, France). Animal treatment was performed according to the recommendations of the French Ethical Committee and under the supervision of authorized investigators. For each experiment, six animals were killed by decapitation, and the kidneys were quickly removed. The adrenal gland was carefully dissected, freed of renal tissue, sliced with scissors, and preincubated in 5 ml Ringer’s solution (100 mM NaCl, 15 mM NaHCO3, 2 mM CaCl2, 2 mM KCl, 15 mM HEPES, 2 mg/ml glucose and 0.3 mg/ml BSA). The Ringer’s solution was gassed with a 95% O2-5% CO2 mixture before use. The perifusion system was set up as previously described (18). Briefly, adrenal fragments were rinsed twice with 5 ml Ringer’s solution, mixed with Bio-Gel P2 (Bio-Rad, Richmond, CA), and transferred into polystyrene columns delimited by Teflon pestels. The perifusion columns were supplied with Ringer’s solution at a constant flow rate (200 µl/min). The pH (7.35) and the temperature (24 C) were kept constant throughout the experiment. The adrenal tissues were allowed to stabilize for 120 min before any test substance was administered. Test substances were dissolved in gassed Ringer’s solution and infused into the columns at the same flow rate as Ringer’s alone by means of a multichannel peristaltic pump (19). Fractions of effluent perifusate were collected every 5 min and frozen until assay. IRL 1038 was dissolved in dimethylsulfoxide (<0.1%). Preliminary experiments have shown that dimethylsulfoxide concentrations up to 1% have no effect on corticosteroid secretion.

Corticosteroid RIAs
Corticosterone and aldosterone concentrations were directly determined in 200-µl aliquots of each perifusion fraction without prior extraction, as previously described (20). Direct measurement of corticosterone and aldosterone was validated by RIA quantification of corticosteroid after HPLC analysis of the effluent perifusate (21). The sensitivity threshold of the assays was 20 pg for corticosterone and 5 pg for aldosterone. For both assays, the intra- and interassay coefficients of variation were 3% and 6%, respectively.

Statistical analyses
Each perifusion pattern represents the mean profile of corticosteroid secretion (± SEM) established over at least three independent experiments. The levels of corticosterone and aldosterone released were expressed as percentages of the basal values, calculated as the mean of eight samples (40 min) taken just before the infusion of the first test substance. Regression analysis (ANOVA) was performed to assess the dose-related inhibition of Ro 47–0203 on ET-1-evoked steroidogenesis, as well as the stimulatory effect of ET-3. Paired and unpaired t tests were used after regression analysis for comparison between values. To compare the net increase in steroid secretion induced by ET-1 in the presence or absence of Ro 47–0203, the areas under the curves were calculated using the trapezoidal rule (22).


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
It has previously been shown that repeated pulses of ET-1 cause attenuation of the response of the adrenal tissue to the peptide (15). To avoid the bias of tachyphylaxis, a single pulse of ET-1 (5 x 10-9 M) was administered to each adrenal slice preparation.

Effect of ETA receptor antagonists
In control conditions, infusion of ET-1 (5 x 10-9 M; 20 min) caused a marked increase in corticosterone (71 ± 7%; Fig. 1AGo) and aldosterone secretion (70 ± 12%; Fig. 1BGo). At a concentration of 3 x 10-6 M, the mixed ETA/ETB receptor antagonist, Ro 47–0203, significantly reduced (P < 0.001) the stimulatory effect of ET-1 on corticosteroid secretion (Fig. 1Go, A and B). The minimum effective dose was 10-6 M (P < 0.05). In contrast, Ro 47–0203 did not affect the response of frog adrenal explants to ACTH (data not shown). Graded doses of Ro 47–0203 caused a concentration-dependent inhibition of corticosterone and aldosterone secretion evoked by ET-1 (Fig. 2Go).



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  		Figure 1. Effect of ET-1 alone or during prolonged infusion of mixed ETA/ETB receptor antagonist Ro 47–0203 on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Top, Control experiments showing effect of ET-1 (5 x 10-9 M; 20 min) on corticosteroid secretion. Bottom, Effect of Ro 47–0203 (3 x 10-6 M) on ET-1-induced steroid secretion. A single pulse of ET-1 (5 x 10-9 M; 20 min) was administered 60 min after beginning of Ro 47–0203 infusion. Profiles represent mean (± SEM) secretion pattern of four independent perifusion experiments. Each point is mean corticosteroid production (expressed as a percentage of spontaneous steroid output) of two consecutive fractions collected during 5 min. Spontaneous level of steroid release (100% basal level) was calculated as mean of eight consecutive fractions (40 min, {circ}) collected before infusion of each dose of test substance. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 17.6 ± 3.5 and 7.9 ± 1.3 pg/min per adrenal gland, respectively.

 


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  		Figure 2. Semilogarithmic plot showing effect of increasing concentrations of Ro 47–0203 on ET-1-induced stimulation of corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. All experimental values were calculated from data similar to those presented in Fig. 1Go. Each point represents mean (± SEM) of four independent experiments. Results are expressed as a percentage of response induced by ET-1 in absence of antagonist. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

 
The stimulatory effect of ET-1 (5 x 10-9 M; 20 min) on corticosterone and aldosterone secretion was totally blocked during prolonged administration of the selective ETA receptor antagonist BQ-485 (10-6 M; Fig. 3Go, A and B). Conversely, BQ-485 had no significant effect on ACTH-evoked corticosteroid secretion (data not shown).



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  		Figure 3. Effect of ET-1 alone or during prolonged infusion of selective ETA receptor antagonist BQ-485 on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Top, Control experiments showing effect of ET-1 (5 x 10-9 M; 20 min) on corticosteroid secretion. Bottom, Effect of BQ-485 (10-7 M) on ET-1-induced steroid secretion. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 18.1 ± 4.1 and 6.3 ± 1.5 pg/min per adrenal gland, respectively. See legend to Fig. 1Go for other designations.

 
Effect of selective ETB receptor agonist and antagonist
Administration of 20-min pulses of the selective ETB receptor agonist IRL 1620 (10-7 and 10-6 M) had no effect on the secretion of corticosterone (Fig. 4AGo) and aldosterone (Fig. 4BGo). In addition, administration of IRL 1620 did not affect the subsequent response of frog adrenal explants to ET-1 (5 x 10-9 M).



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  		Figure 4. Effect of two pulses of ETB receptor agonist IRL 1620 (10-7 and 10-6 M) and one pulse of ET-1 (5 x 10-9 M) on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Each pulse of secretagogue was administered during 20 min. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 12.0 ± 1.0 and 10.0 ± 2.0 pg/min per adrenal gland, respectively. See legend to Fig. 1Go for other designations.

 
The ETB receptor antagonist IRL 1038 (10-6 M) caused by itself a modest and transient stimulation of corticosteroid secretion (Fig. 5Go, A and B). Nevertheless, prolonged administration of IRL 1038 did not significantly modify the corticotropic effect of ET-1 (Fig. 5Go, A and B).



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  		Figure 5. Effect of ET-1 alone or during prolonged infusion of ETB receptor antagonist IRL 1038 on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Top, Control experiments showing effect of ET-1 (5 x 10-9 M; 20 min) on corticosteroid secretion. Bottom, Effect of IRL 1038 (10-6 M) on ET-1-induced steroid secretion. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 14.5 ± 1.4 and 9 ± 1.1 pg/min per adrenal gland, respectively. See legend to Fig. 1Go for other designations.

 
Effect of ET-3 on corticosteroid production
Administration of graded concentrations of ET-3 (10-8 to 5 x 10-7 M) to perifused adrenal slices induced a dose-related increase in corticosterone and aldosterone secretion (Table 1Go). The minimum effective dose was 5 x 10-8 M (P < 0.01) and the maximum stimulation was obtained with a concentration of 10-7 M ET-3. The dose-response curves showed that ET-3 was less potent than, but as efficient as ET-1 in stimulating corticosterone and aldosterone secretion (Fig. 6Go).


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  		Table 1. Effect of graded concentrations of ET-3 on secretion of corticosterone and aldosterone by perifused frog adrenal explants

 


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  		Figure 6. Semilogarithmic plot comparing effect of increasing concentrations of ET-1 (10-11 to 10-8 M) and ET-3 (10-8 to 5 x 10-7 M) on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Results are expressed as a percentage of basal secretory rate.

 
Effect of selective ETA and ETB receptor antagonists on ET-3-evoked corticosteroid production
The stimulatory effect of ET-3 (10-7 M; 20 min) on corticosterone (98 ± 6%) and aldosterone secretion (97 ± 5%) was abolished during administration of the selective ETA receptor antagonist BQ-485 (10-7 M; Fig. 7Go, A and B). In contrast, the selective ETB receptor antagonist IRL 1038 (10-6 M) did not affect the corticotropic response to ET-3 (Fig. 8Go, A and B).



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  		Figure 7. Effect of ET-3 alone or during prolonged infusion of selective ETA receptor antagonist BQ-485 on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Top, Control experiments showing effect of ET-3 (10-7 M; 20 min) on corticosteroid secretion. Bottom, Effect of BQ-485 (10-7 M) on ET-3-induced steroid secretion. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 9.5 ± 0.8 and 7.8 ± 0.9 pg/min per adrenal gland, respectively. See legend to Fig. 1Go for other designations.

 


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  		Figure 8. Effect of ET-3 alone or during prolonged infusion of ETB receptor antagonist IRL 1038 on corticosterone (A) and aldosterone secretion (B) by perifused frog adrenal explants. Top, Control experiments showing effect of ET-3 (10-7 M; 20 min) on corticosteroid secretion. Bottom, Effect of IRL 1038 (10-6 M) on ET-3-induced steroid secretion. Mean basal levels of corticosterone and aldosterone secretion in these experiments were 13.5 ± 0.6 and 7.7 ± 0.3 pg/min per adrenal gland, respectively. See legend to Fig. 1Go for other designations.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In contrast to mammals, the frog adrenal gland does not exhibit any zonation, but is composed of steroidogenic cells intermingled with chromaffin cells (23, 24). In addition, the frog adrenal tissue is richly vascularized (25, 26, 27). Because endothelins exert biological activities on adrenocortical, chromaffin, and vasculature cells (1, 15, 28, 29, 30, 31), membrane binding studies would not be appropriate to characterize the receptor involved in the corticotropic action of ETs in amphibians. We have, therefore, applied a functional approach (i.e. measurement of corticosteroid secretion) to determine the type of receptor mediating the effect of ETs on frog adrenocortical cells.

The present study clearly demonstrates that the corticotropic activity of ETs on frog adrenal explants is mediated through a receptor subtype closely related to mammalian ETA receptors. 1) The stimulatory effect of ET-1 was markedly reduced by the mixed ETA/ETB receptor antagonist Ro 47–0203 (8) and totally abolished by the selective ETA receptor antagonist BQ-485 (32). In contrast, the response to ET-1 was not affected by the selective ETB receptor antagonist IRL 1038 (33). Interestingly, IRL 1038, the cyclic C-terminal 11–21 fragment of ET-1, caused a slight stimulation of corticosteroid secretion but did not induce any desensitization phenomenon, suggesting that this analog may not exert its agonistic activity through the ETA receptor. 2) The selective ETB receptor agonist IRL 1620 (34), even at high concentrations (10-7 or 10-6 M), did not mimic the stimulatory effect of ET-1. In addition, after two successive pulses of IRL 1620, the response of adrenal explants to ET-1 was not affected, indicating that the ETB agonist, in contrast to ET-1, did not cause desensitization of the receptor. 3) Although ET-3, an ETC receptor-preferring agonist (12), induced a dose-dependent stimulation of corticosterone and aldosterone secretion by perifused frog adrenal explants, the peptide was 400 times less potent than ET-1. In addition, the stimulatory effect of ET-3 was totally blocked by the ETA receptor antagonist BQ-485, but was not reduced by the ETB receptor antagonist IRL 1038, indicating that the action of ET-3 can be accounted for by its weak agonistic activity on ETA receptors.

In mammals, autoradiographic studies and RT-PCR experiments have shown the expression of the ETA and ETB receptor subtypes in the adrenal cortex (31, 35, 36). In particular, glomerulosa cells that are the mammalian counterpart of amphibian adrenocortical cells (37), possess both ETA and ETB receptors (31, 36). In rat, it has been reported that the direct stimulatory effect of ET-1 on aldosterone secretion can be accounted for by activation of either the ETB receptors only (31, 38) or both the ETA and ETB receptors (39, 40), whereas the ETA receptors mediate the stimulatory effect of ET-1 on glomerulosa cell proliferation (41, 42). These findings, together with the present report, reveal the occurrence of possible species differences in the mode of action of ETs on adrenocortical cells in vertebrates.

In conclusion, the present study demonstrated that in the frog the stimulatory effect of ETs on corticosteroid secretion is mediated by a receptor subtype that exhibits the same pharmacological characteristics as the mammalian ETA receptor. The frog adrenocortical tissue, which is composed of a single population of steroid-producing cells (43), thus appears as a valuable model in which to investigate the transduction mechanisms associated with the activation of ETA receptors in an endocrine cell.


   Acknowledgments
 
We thank Dr. D. Duterte-Boucher (CNRS UPRES-A 6036, Rouen, France) for valuable advice on statistical analysis. Bosentan (Ro 47–0203) was kindly provided by Dr. Martine Clozel (Hoffmann-La Roche, Basel, Switzerland).


   Footnotes
 
1 This work was supported by grants from the Institut National de la Santé et de la Recherche Médicale (U 413), the Direction des Recherches et Etudes Techniques (92–099), the Ministère des Affaires Etrangère (PV-P-73–9), and the Conseil Régional de Haute-Normandie. Back

2 Affiliated Professor at the INRS-Santé, Montréal. Back

Received April 3, 1997.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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