Functional characterization of basolateral and
luminal dopamine receptors in rabbit CCD
Osamu
Saito,
Yasuhiro
Ando,
Eiji
Kusano, and
Yasushi
Asano
Division of Nephrology, Department of Medicine, Jichi Medical
School, Tochigi 329-0498, Japan
 |
ABSTRACT |
Previous studies reported the existence
of both D1- and D2-like receptors in the
cortical collecting duct (CCD). However, especially with regard to
natriuresis, it remains controversial. In the present study, rabbit CCD
was perfused to characterize the receptor subtypes responsible for the
tubular actions. Basolateral dopamine (DA) induced a dose-dependent
depolarization of transepithelial voltage. Basolateral domperidone, a
D2-like receptor antagonist, abolished depolarization,
whereas SKF-81297, a D1-like receptor agonist, showed no
significant change. In addition, bromocriptine, a D2-like
receptor agonist, also caused depolarization, whereas SKF-81297, a
D1-like receptor agonist, did not depolarize significantly. Moreover, RBI-257, a D4-specific antagonist, reversed the
basolateral DA-induced depolarization. In contrast to the basolateral
side, luminal DA caused depolarization via a D1-like
receptor; however the change was less than that for basolateral DA. For
further evaluation, 22Na+ flux
(JNa) was measured to confirm the effect of DA
on Na+ transport. Basolateral DA also caused a suppression
of JNa, and this reaction was abolished by
domperidone. These results suggested that the basolateral
D2-like receptor is mainly responsible for the natriuretic
action of DA in rabbit CCD.
in vitro microperfusion; transepithelial voltage; dopamine
receptor; sodium transport; cortical collecting duct
 |
INTRODUCTION |
DOPAMINE (DA)
CAUSES NATRIURESIS in various mammals, such as dogs, rats,
rabbits, and humans (11, 22, 24). An increase in
glomerular filtration rate (GFR) is a definite factor in natriuresis. In addition, DA causes vasodilatation of the renal artery, and this is
the major mechanism for increasing GFR. As an endogenous catecholamine,
DA also has been shown to inhibit angiotensin II-induced mesangial cell
contraction (8). A physiological role of DA in glomerular
contractility is supported by the presence of dopaminergic nerve
endings close to the vascular pole of the glomeruli and juxtaglomerular
cells (9).
With regard to electrolyte metabolism, DA directly suppresses tubular
sodium reabsorption with a resultant increase in fractional excretion
of sodium by inhibiting the activity of
Na+-K+-ATPase in several nephron
segments and also by suppressing the apical
Na+/H+ exchange in the proximal tubule
(6). The first two subsegments of the proximal tubule,
i.e., S1 and S2, produce DA from L-dopa by the action of
aromatic L-amino-acid decarboxylase. Proximal convoluted
tubule also secretes the DA to basolateral and luminal sides
(7). Thus the proximal convoluted tubule-derived DA can act as a paracrine factor at adjacent and more distal segments (37). In the medullary thick ascending limb of the loop of
Henle, dopamine- and cAMP-regulated phosphoprotein (DARPP-32) has been identified in the kidney of rat, mouse, and rabbit (23).
This is another line of evidence that DA, as an endogenous hormone, may
regulate the distal nephron functions. Indeed, in the collecting ducts,
DA has been reported to inhibit sodium reabsorption (15, 17).
The dopamine receptor family is divided into two major groups
with pharmacological and molecular character, the D1-like
and D2-like dopamine receptors, respectively (34,
35). The D1-like receptors (D1 and
D5) couple to the G protein Gs and activate adenylyl cyclase. The D2-like receptors (D2,
D3, and D4) are prototypical G protein-coupled
receptors that inhibit adenylyl cyclase (Gi) and activate
K+ channels (18, 36). All subtypes of the
dopamine receptors are expressed in the kidney (14, 25,
31). In the rat cortical collecting duct (CCD), the
D1 receptor has been detected by in situ hybridization or
immunohistochemistry (27). Also, Satoh, et al.
(32) have shown that DA decreases Na+-
K+-ATPase activity in the CCD and medullary thick ascending
limb of the rat. On the other hand, physiological studies suggested the
presence of the D2-like receptor in rat (39)
and rabbit CCD (26, 40). Thus there still is controversy
concerning the dominant receptor subtype in this segment. In addition,
the polarity of the dopamine receptor localization, i.e., basolateral
or luminal side of the tubule, remains unexplored.
In the present study, rabbit CCD was perfused in vitro, and the
response of transepithelial voltage (Vt) and
Na+ transport (JNa) to basolateral
and luminal DA was examined to characterize the subtypes and
localization of the DA receptors.
 |
METHODS |
In vitro microperfusion.
Single CCDs were dissected from kidneys of anesthetized (intravenous
pentobarbital sodium, 1 mg/kg) female Japanese White rabbits, weighing
1.5-2.5 kg and perfused in a Lucite bath chamber on the stage of
an inverted microscope at 37°C using the methods described previously
(2, 5). To facilitate luminal perfusate exchange during
each experiment, a polyethylene tube (PE-10; Clay-Adams, Parsippany,
NJ) was placed inside pipette B, which was connected to the
tubular lumen for perfusion. The luminal perfusate flow rate was
adjusted by hydrostatic pressure. Luminal perfusate exchange was
performed manually by injecting perfusate into the polyethylene tube,
washing out the preexisting medium in pipette B.
The composition of bath medium and isotonic luminal perfusate was as
follows (in mM): 105 NaCl, 25 NaHCO3, 10 sodium acetate, 2.3 Na2HPO4, 10 NaH2PO4, 5 KCl, 1.8 CaCl2, 1.0 MgSO4, 8.3 glucose, and 5 alanine (osmolality 300 mosmol/kgH2O).
Before use, all solutions were bubbled to equilibration at 37°C with
a 95% O2-5% CO2 gas mixture to achieve a pH
of ~7.40 and a PCO2 of ~40 Torr. Bath
medium was continuously exchanged during the experiment at a flow rate
of 25 ml/h by using a syringe pump (model STC-521, Terumo, Tokyo,
Japan). To exchange bath medium, 2 ml of new bath medium, which was
warmed to 37°C, were rapidly infused three times into the bath
chamber through another set of syringe and polyethylene tubing. This
maneuver was completed within 30 s. Luminal perfusates were also
shielded in plastic syringes until use. The pH of the solutions was
checked again each time just before use by a pH meter (model M-220,
Corning, NY).
Experiments were started after perfusion of tubules for 60-90 min
at 37°C to obtain a stable Vt and to eliminate
residual actions of endogenous arginine vasopressin (AVP; equilibration period) (4). To detect cell damage and perfusate leak,
luminal perfusates contained 0.2 mg/ml FD&C green dye. Appearance of
the tubular cells and dye leakage were continuously monitored under the
microscope. Tubules with dye leakage or an increasing number of cells
stained with the dye were discarded.
Measurement of Vt.
The voltage difference between two calomel cell electrodes connected by
Ringer-agarose bridges to the bath medium and perfusate in
pipette B, respectively, was continuously monitored by an
electrometer (model MEZ-8201, Nihon Kohden, Tokyo, Japan) by using
standard techniques and recorded on a chart (model R202, Rikadenki,
Tokyo, Japan).
When Vt (in mV) was exclusively measured, a high
perfusion rate (~30 nl/min) was chosen, and the perfused fluid was
collected in a large-volume (~10-µl) pipette to avoid changes in
perfusion rate and perfusion pressure that might affect
Vt during exchange or collection of luminal
perfusate. After the equilibration period, stability of the
Vt was confirmed by exchanging the luminal
perfusate for that containing vehicle alone. Because
Vt was significantly different from tubule to
tubule (
5 to
30 mV), when appropriately adequate for comparison,
the degree of depolarization (%Vt change) was
calculated from the Vt at maximal depolarization
(Vt dep, max) and the corresponding
basal Vt (Vt, basal) as
follows
Agonists and antagonists.
DA agonists and antagonists exert various binding specificities to the
D1- and D2-like receptors (1, 19, 20, 25, 43).
In the present study, we used SKF-81297, a D1 and D5
agonist, as a D1-like receptor agonist and SCH-23390, a
D1 and D5 antagonist, as a D1-like
receptor antagonist. With reference to the D2-like receptor, we chose bromocriptine, a D2-like receptor
agonist (D2, D3, and, partially, a
D4 agonist) and domperidone (D2,
D3, and D4 antagonist) as a D2-like
receptor antagonist, respectively (33, 34, 35, 38). For
further confirmation of D2-like receptor subtype, a
specific D4 receptor antagonist, RBI-257, was also used
(19). Their pharmacological profiles are shown in Table
1. All these reagents were purchased from
Sigma (St. Louis, MO).
Effect of DA on Na+ transport.
In this series of experiments, 22NaCl (DuPont, Wilmington,
DE) was added to the luminal perfusate as a tracer. Lumen-to-bath Na+ efflux, JNa
(peq · min
1 · mm tubule
1),
was calculated from the disappearance rate of
22Na+ from the luminal perfusate according to
the following equations
|
(1)
|
|
(2)
|
where Vo is the collection rate (in
nl/min); Vp and t are the volume of
the constriction pipette and collection time, respectively; Ki and Ko are the
concentrations of Na+ in the perfusate and collected fluid,
respectively; and L is the length of the tubule, which was
measured directly at the end of each experiment with the eyepiece
reticule. The radioactivity of 22Na+ was
counted by using a liquid scintillation counter (Auto-Gamma 5650, Packard Japan, Tokyo, Japan).
After the equilibration period mentioned above, two or three
collections were made (basal period). Then, in 10-15 min, when Vt depolarization was stabilized after addition
of DA, three collections were made (experimental period).
To detect the reverse leakage of the bath medium into the tubular
lumen, 22Na+ activity of the first one or two
basal collections was counted immediately. If leakage was suggested by
an unusually low count rate, compared with those in the previous time
control experiments (30), the experiment was discontinued,
although leakage was not observed in the present series of experiments.
Statistics.
Data are presented as means ± SE. Unless specified otherwise,
differences among groups were assessed by analysis of variance (Scheffé's post hoc test for multiple comparisons), using
Statview 5.0J software. A difference with a P value of
<0.05 was considered significant.
 |
RESULTS |
Effect of basolateral DA on Vt.
Basolateral DA (1 nM-10 µM) induced dose-dependent
depolarization of Vt (26.3 ± 2.8, 44.3 ± 5.3, and 75.1 ± 6.9%, respectively) (Figs.
1 and 2).
To evaluate the receptor subtype, basolateral DA was applied after the
pretreatment with 10 µM basolateral SCH-23390, an antagonist of both
the D1 and D5 receptors, or 10 µM basolateral domperidone, a D2-like receptor antagonist that antagonizes
all D2, D3, and D4 receptors (Table
1). In the presence of SCH-23390, which by itself did not change
Vt, the depolarization induced by DA was not
significantly altered (28.7 ± 8.2% at 100 nM, 49.3 ± 9.3%
at 10 µM) (Figs. 3A and
4A). On the other hand, the
DA-induced depolarization was significantly suppressed in the
presence of domperidone, which by itself did not alter the
Vt (1.2 ± 0.5% at 100 nM, 20.8 ± 4.2% at 10 µM, n = 5) (Figs. 3B and
4B).

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Fig. 2.
Dose-dependent change in Vt
(%Vt change) in response to basolateral DA
(n = 8). P value vs. basal
Vt is shown.
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Fig. 3.
Original trace of the Vt change
induced by basolateral DA in the presence of basolateral SCH-23390
(D1-like, both D1 and D5
antagonist; A) or domperidone (D2-like,
D2, D3, and D4 antagonist;
B).
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Fig. 4.
Effect of basolateral DA on
Vt in the presence of basolateral SCH-23390
(D1-like antagonist) or domperidone (D2-like
antagonist). A: pretreatment with basolateral SCH-23390.
, basolateral DA alone (adapted from Fig. 2);
, basolateral DA superimposed on SCH-23390; NS, not
significant vs. basolateral DA alone (by nonpaired t-test).
SCH-23390 did not significantly alter the basolateral DA-induced
depolarization. *P < 0.01 vs. basal.
**P < 0.001 vs. basal (n = 5).
B: pretreatment with basolateral domperidone.
, basolateral DA alone (adapted from Fig. 2);
, basolateral DA superimposed on domperidone.
Domperidone significantly suppressed the basolateral DA induced
depolarization. P < 0.001 vs. same concentration of
basolateral DA alone (by nonpaired t-test).
***P < 0.01 vs. basal (n = 5).
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For further confirmation, agonist studies were performed. Basolateral
SKF-81297 (10 µM), which agonizes both the D1 and
D5 receptors (Table 1), induced no significant
Vt change (3.5 ± 3.8% at 100 nM and
5.6 ± 5.8% at 10 µM) (Figs.
5A and
6), whereas 100 nM and 10 µM
basolateral bromocriptine, a D2-like receptor agonist (mainly of
D2 and D3 and, partially, of D4)
(Table 1), caused a dose-dependent depolarization (21.7 ± 5.8%
at 100 nM and 33.5 ± 5.1% at 10 µM, n = 6)
(Figs. 5B and 6). These results demonstrated that
basolateral DA causes depolarization of the Vt
not via a D1-like receptor but via a D2-like
receptor.

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Fig. 5.
Original trace of the Vt change
induced by basolateral SKF-1297 (D1-like agonist; both
D1 and D5 agonist; A) or
bromocriptine (D2-like; D2, D3, and
partially D4 agonist; B). Bromocriptine but not
SKF-81297 mimicked the basolateral DA-induced depolarization.
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Fig. 6.
Effect of basolateral SKF-81297 (D1-like
agonist) or bromocriptine (D2-like agonist) on
Vt . *P < 0.05 and
**P < 0.005 vs. basal Vt
(n = 6).
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|
As recent papers suggested the existence of a D4 receptor
in CCD (39, 40), we performed further evaluation for the
subtype of the basolateral D2-like receptor. DA was applied
in the presence of basolateral RBI-257, a specific D4 receptor
antagonist (19). Basolateral RBI-257 (10 µM) did not
change the Vt by itself, whereas it abolished
the action of 100 nM and 10 µM basolateral DA. After washing out of
RBI-257, significant depolarization was observed with a 10 µM
basolateral DA rechallenge (100 nM DA with RBI-257, 2.2 ± 0.4%;
10 µM DA with RBI-257, 5.2 ± 0.5%; 10 µM basolateral DA
rechallenge, 73.2 ± 5.1%, respectively; n = 5)
(Fig. 7).

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Fig. 7.
Effect of basolateral RBI-257 (D4-specific antagonist) on
basolateral DA-induced depolarization. RBI-257 blocked basolateral
DA-induced depolarization completely. *P < 0.001 vs. basal Vt (n = 5).
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Effect of luminal DA on Vt.
Next, we investigated whether luminal DA exerts an effect on
Vt. Because urinary concentration of DA is
10-100 times higher than that at the plasma level
(41), we chose higher concentrations for luminal study.
Although 1 µM luminal DA did not cause a significant depolarization
(0.2 ± 2.5%; n = 8), 10 and 100 µM luminal DA
depolarized Vt significantly (14.6 ± 6.5%
at 10 µM, 18.2 ± 6.8% at 100 µM, respectively,
n = 8) (Figs. 8 and
9). Pretreatment with 10 µM luminal
SCH-23390 did not change Vt by itself (4.1 ± 2.2%; n = 4); however, it completely blocked the
luminal DA-induced depolarization (5.6 ± 3.7%; n = 4) (Fig. 10A). In
contrast, 10 µM luminal domperidone, which also did not affect
Vt by itself (0.2 ± 1.2%;
n = 4), failed to suppress the luminal DA-induced
depolarization (37.5 ± 4.9%; n = 4) (Fig.
10B). In good agreement with these antagonist studies, 10 µM luminal SKF-81297 mimicked the effect of luminal DA, whereas 10 µM luminal bromocriptine had no significant effect (37.7 ± 6.3% with luminal SKF-81297,
8.3 ± 7.5% with luminal
bromocriptine; n = 6) (Figs.
11 and
12).

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Fig. 9.
Dose-dependent change in Vt in response to
luminal DA. Luminal DA (1 µM) did not alter
Vt, whereas 10 and 100 µM luminal DA
depolarized Vt significantly (P < 0.01 vs. basal, n = 8.)
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Fig. 10.
Effect of luminal DA on
Vt in the presence of luminal SCH-23390
(D1-like antagonist) or domperidone (D2-like
antagonist). A: pretreatment with luminal SCH-23390.
SCH-23390 significantly suppressed the 10 µM luminal DA-induced
depolarization (n = 4). B: pretreatment with
luminal domperidone. Domperidone did not prevent the 10 µM luminal
DA-induced depolarization (n = 4).
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Fig. 11.
Original trace of the Vt change induced by
luminal bromocriptine (D2-like agonist) or SKF-81297
(D1-like agonist). SKF-81297 but not bromocriptine mimicked
the luminal DA-induced depolarization.
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Fig. 12.
Effect of luminal bromocriptine
(D2-like agonist) or SKF-81297 (D1-like
agonist) on Vt. Luminal SKF-81297 but not
bromocriptine caused depolarization. P value vs.
basal Vt is shown (n = 6).
|
|
Thus, like basolateral DA, luminal DA also induced depolarization of
the Vt. However, the receptor subtype
responsible for this action was not a D2-like receptor but
a D1-like receptor. Besides the difference in receptor
subtype, it was noted that the depolarization induced by luminal DA
required 10,000 times higher concentrations (>10 µM) than those for
basolateral DA (>1 nM). Also, the depolarization itself was much
smaller than that induced by basolateral DA. Namely, at 10 µM,
basolateral and luminal DA depolarized Vt by 75 and 15%, respectively (Fig. 2 vs. Fig. 9).
Effect of the DA function on Na+ transport.
It is known that the Vt in CCD primarily
represents lumen-to-basolateral Na+ flux (16).
To explore the mechanism of basolateral DA-induced depolarization, we
performed an Na+ flux study. In the presence of 100 nM and
10 µM basolateral DA, JNa was significantly
decreased (basal, 51.4 ± 4.2; 100 nM, 44.9 ± 3.2; 10 µM,
32.0 ± 2.9 peq · min
1 · mm
tubule
1, respectively) (Fig.
13A). Pretreatment with 10 µM basolateral domperidone reversed the DA-induced suppression of
JNa (basal, 49.2 ± 3.8; domperidone
alone, 48.5 ± 1.6; 10 µM DA with domperidone, 46.6 ± 3.5 peq · min
1 · mm tubule
1,
respectively) (Fig. 13B).

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Fig. 13.
Effect of basolateral DA on Na+ efflux
(JNa). A: changes in
Vt and JNa induced by
basolateral DA. Basolateral DA suppressed JNa.
*P < 0.01 vs. basal. ** P < 0.001 vs.
basal. P < 0.01 vs. 100 nM DA (n = 6). B: effect of basolateral DA in the presence of
basolateral domperidone (D2-like antagonist)
(n = 6). In the presence of basolateral 10 µM
domperidone, the effect of 10 µM basolateral DA was abolished. Thin
lines in JNa represent individual experiments.
|
|
In contrast, however, 100 µM luminal DA caused no significant change
in JNa despite significant depolarization of
Vt at 100 µM (data not shown).
 |
DISCUSSION |
In rat CCD, the presence of a D1-like receptor has
been reported (29, 42), whereas some previous studies
demonstrated D2-like receptor activity in the same segment
of the rabbit and the rat (26, 39). Also, in vivo studies
suggested that D2-like receptors are responsible for
natriuresis (12, 17). Differences between animal species
may be one of the reasons for the discrepancy. In addition, polarized
localization of different DA receptors in the apical and basolateral
side of the epithelium may exist, like AVP or PGE2
(2, 3, 5, 13), yielding conflicting results in the
previous studies. Indeed, apical DA receptors have been reported in the
proximal tubules (10) as well as in the collecting duct
(28, 40).
To characterize receptor subtypes of DA in the rabbit CCD, we thus
applied DA not only from the basolateral side but also from the luminal
side. It was considered that the DA receptor resides on both sides of
the CCD epithelium. Namely, DA depolarized the
Vt not only when applied from the basolateral
side but also from the luminal side of the CCD. Interestingly, however,
the depolarization was mediated by distinct subtypes of the DA
receptor. From the basolateral side, DA appeared to induce
depolarization via a D2-like receptor. The
D2-like receptor includes D2, D3, and D4 receptor subtypes (34, 35). Our
basolateral agonist study showed that the D2-like receptor
was dominant, and the basolateral antagonist study also confirmed this
result. Moreover, the D4 subtype seemed to be the major
basolateral DA receptor (Fig. 7). However, concerning
D2-like receptor subtypes, these results seemed slightly
discrepant because bromocriptine agonizes the D2-like receptor (mainly via D2 and D3 receptors), and
the affinity of the D2 and D3 receptors is
nearly 10-100 times higher than that of the D4
receptor (Table 1). However, DA itself also indicated a much lower
affinity to the D4 receptor than to the D2 and
D3 receptors. Indeed, the affinity of DA to the
D4 receptor has been shown to be only 10 times higher than
that of bromocriptine (33, 38). In our results, RBI-251
showed complete inhibition of the effects of basolateral DA.
Interestingly, RBI-251 is a D4-specific antagonist. If the
D2 or D3 receptor existed mainly in the
basolateral CCD, DA might cause the significant depolarization in the
presence of RBI-251. Thus we concluded that basolateral DA caused
depolarization via a D2-like receptor, especially to the
D4 subtype.
In contrast, the D1-like receptor is the major apical
DA receptor. Because there is no adequate antagonist or agonist to
distinguish D1 and D5 receptors available at
present (25, 33, 38), in this study we could not specify
the subtype of the D1-like receptor on the apical side.
In rat CCD, only D3 and D4 receptor subtypes
have been demonstrated by in situ hybridization studies (28,
40). The D3 receptor resides exclusively on the
apical side (28), whereas D4 receptor
immunostaining was found on both sides of the epithelia (40). These discrepancies between rat and rabbit argue for
the species difference in DA receptor subtype in the CCD.
With respect to the role of basolateral and luminal DA receptors in
Na+ transport, the present study demonstrated that
basolateral DA receptors are primarily responsible for the inhibition
of Na+ transport. Although luminal DA caused modest
depolarization at concentrations >10 µM (Fig. 9), it failed to cause
a significant suppression of Na+ transport (data not
shown). Thus the mechanism of depolarization induced by luminal DA
remains unknown. However, a similar Na+-independent change
in Vt has been noted in rabbit CCD when AVP is
applied from the luminal side (5). Luminal AVP has been shown to suppress H+ secretion in this segment
(21). Therefore, luminal DA may depolarize the
Vt by modulating electrogenic transport other
than that of Na+. Further studies are needed to evaluate
the regulation between basolateral and luminal DA.
 |
ACKNOWLEDGEMENTS |
We thank Yukie Akutsu and Hiromi Kasakura for expert
assistance in the experiments and Dr. Takako Saito for thoughtful suggestions.
 |
FOOTNOTES |
This study was supported in part by Grants-in-Aid for Scientific
Research from the Ministry of Education, Science and Culture, Japan
(nos. 06671147 and 08671294). Portions of this paper were presented at
the 27th Annual Meeting of the American Society of Nephrology in New
Orleans, LA, 1996.
Address for reprint requests and other correspondence: Y. Ando,
Div. of Nephrology, Dept. of Medicine, Jichi Medical School, 3311-1 Yakushiji Minamikawachi-machi, Tochigi 329-0498, Japan.
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.
Received 22 October 1999; accepted in final form 22 February 2001.
 |
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