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2-Adrenoceptor–Mediated Modulation of Jejunal Epithelial Transport in Young and Adult Rats1
Institute of Pharmacology and Therapeutics, Faculty of Medicine, 4200 Porto, Portugal
2To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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2-adrenoceptor activation in young
(20-d-old) and adult (60-d-old) rats, using short-circuit
(Isc) measurements in the absence or presence of furosemide
(1 mmol/L). The effect of 2-adrenoceptor stimulation by
5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine
(UK 14,304; 0.3–3000 nmol/L) was a concentration-dependent
decrease in Isc with similar half-maximal effective
concentration (EC50; 12.3 ± 1.1 vs. 9.6 ± 1.1
nmol/L) and maximal effect (Emax; 70.6 ± 6.9 vs. 80.6
± 4.5% of reduction) values in adult food-deprived and fed
rats. The effect of UK 14,304 on Isc in fed and
food-deprived rats was markedly (P < 0.05)
attenuated by furosemide (1 mmol/L). Emax values for UK
14,304 in 20-d-old food-deprived rats were higher (P
< 0.05) than those observed in fed rats (93.3 ± 3.3 vs.
67.0 ± 11.3% of reduction), without differences in
EC50 values. The effect of UK 14,304 on Isc in
20-d-old fed rats was completely abolished by furosemide (1 mmol/L). In
food-deprived young rats, the effect of UK 14,304 was also markedly
(P < 0.05) antagonized by furosemide, but not
completely abolished. Specific [3H]-rauwolscine binding
in membranes from jejunal epithelial cells revealed the presence of a
single class of binding sites, with an apparent
KD in the low nmol/L range. In 20-d-old
food-deprived rats, specific [3H]-rauwolscine binding
was markedly increased, and this was reversed by refeeding.
Na+,K+-ATPase activity in isolated jejunal
epithelial cells from 60-d-old fed rats was twice that in 20-d-old fed
rats [117 ± 14 vs. 52 ± 5 nmol free inorganic phosphorus/(mg
protein·min)]. Food deprivation in adult rats, but not in 20-d-old
rats, was accompanied by a significant decrease in
Na+,K+-ATPase activity. In both young and adult
rats (fed and food-deprived), UK 14,304 did not affect
Na+,K+-ATPase activity. In conclusion, food
deprivation in 20-d-old rats enhanced the response to
2-adrenoceptor stimulation. This effect, which depends
primarily on the stimulation of a furosemide-sensitive
antisecretory mechanism, is suggested to result from increases in the
number of jejunal epithelial 2-adrenoceptors.
KEY WORDS: • rat jejunum • 2-adrenoceptors • Na+,K+,2Cl--co-transporter • Na+K+-ATPase
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). These factors,
related to enteral nutrition, play a key role in the modulation of
gastrointestinal function. It is not only the presence of food, but
also the absence of luminal contents in the gastrointestinal tract that
has the capacity to influence intestinal function, comprising both
absorptive and secretory mechanisms. Although the factors directly
responsible for such changes have not been detailed, it is believed
that the effect is due not to systemic influences associated with
fasting conditions, but to the reduction in contact between the
intestinal mucosa and luminal contents (Carey and Cooke 1992
, Carey et al. 1994
). Food deprivation has
been shown to change intestinal mucosal structure as well as function
(Johnson 1988
, Williamson 1978
). Studies
performed in rats deprived of food for a period of 24–48 h
(Young and Levin 1990a
and 1990b
) and ground squirrels
(48–72 h) (Carey 1992
) showed that the jejunum and
ileum became hyperactive to a variety of stimuli that elicit intestinal
secretion, despite the decreasing cell population of crypts and villi.
In addition, the intestine of food-deprived animals is endowed with
enhanced absorptive capacity, most likely as the result of an increase
in enterocyte maturity and decrease in cell proliferation
(Thompson and Debnam 1986
, Young and Levin 1990a
).
The driving force for fluid absorption in the mammalian small intestine
is the active transport of Na+, and
Cl-, which may be electrically silent
(Frizzell et al. 1979
) or which may involve electrogenic
Na+ transport (Esposito 1984
). In
addition, there is active secretion of Cl-
accompanied by Na+ and water (Rao and Fields 1983
). Studies on the neurohumoral control of intestinal
transport showed that catecholamines stimulate electrolyte absorption
and inhibit anion secretion in the small and large intestines
(Field and McColl 1973
, Sellin and DeSoignie 1984
). The proabsorptive and antisecretory effect of
catecholamines has been attributed to the activation of
-adrenoceptors. Liu and Coupar (1997)
suggested that
the 2-adrenoceptors involved in the
antisecretory actions in the rat intestinal epithelium are of the
2D or 2A subtype. All
of these observations are supported by radioligand studies that
demonstrated the presence of 2-adrenoceptors
in enterocyte membranes (Chang et al. 1982
and 1983
,
Cotterell et al. 1984
, Nakaki et al. 1983
, Tanaka and Starke 1979
).
During postnatal development, rats gradually shift from a low
carbohydrate, high fat and low salt intake to one that is high
carbohydrate, low fat and high salt (Buddington and Diamond 1989
). To digest and absorb nutrients properly, the small
intestine adapts by regulating membrane properties, enzyme activities
and transporter activities at levels capable of processing diets
typically consumed at each developmental stage (Buddington and Diamond 1989
, Meddings and Theisen 1989
).
Na+,K+-ATPase is one of the
enzymes localized at the basolateral enterocyte membrane that perform a
very important role in intestinal physiology by setting the ionic
gradients necessary for absorptive and secretory mechanisms. The basal
activity and modulation of this ionic pump has been shown in rats to
depend on several factors: 1) dietary salt level,
2) age of the rats and 3) stage of development
(Binder 1983
, Finkel et al. 1994
,
Lucas-Teixeira et al. 2000
, Vieira-Coelho et al. 1998
). In addition to the sodium pump, other membrane
transporters are involved in the vectorial movement of ions across the
intestinal epithelium; for example, the
Na+,K+,2Cl-
co-transporter
(NKCC)3
is very important for establishing the Cl-
gradient necessary for its secretion at the apical membrane
(Binder 1983
, Esposito 1984
,
Frizzell et al. 1979
).
The modulation by 2-adrenoceptors of jejunal
electrolyte transport has not yet been analyzed in detail in young rats
(20 d old) vs. adult rats (60 d old) in fed and food-deprived
states. This study reports that the effect of
2-adrenoceptor activation on the
short-circuit current (Isc) is mediated
through a furosemide-sensitive pathway and therefore depends on the
ionic gradients generated by the NKCC co-transporter, and that this
effect is affected by food deprivation.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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All of the experiments were performed in male Wistar rats (Harlan-Interfauna, Barcelona, Spain), 20 d old (40–50 g) and 60 d old (260–300 g). Adult rats were divided in two groups as follows: 1) rats fed a standard nonpurified diet [rat maintenance diet (fat 2.2%, protein, 15.0%, fiber, 5.2%), catalog number 9609 obtained from Harlan-Teklad, Oxon, UK] and 2) rats deprived of food for 48 h. Young rats were also divided in two groups as follows: 1) breast-fed rats that were kept with their dams and 2) rats deprived of food for 24 h. All rats consumed tap water ad libitum. The Scientific Review Board of the Foundation for Science and Technology (Portugal) approved the experimental protocol.
Preparation of stripped jejunal epithelial sheets.
Rats were killed by decapitation while under ether anesthesia, and
three jejunal segments located 10–15 cm distal from the pyloric
sphincter were removed. Each segment (2 cm long) of jejunum was cut
longitudinally along the mesenteric border, washed free of luminal
contents and the tissue pinned mucosal side down on a dental wax block.
The serosa and muscularis were stripped away by dissection to obtain
the epithelial sheets, as described previously (Nellans et al. 1974
). Three adjacent pieces were routinely prepared from a
single jejunum.
Experimental procedure.
Epithelial sheets were mounted in Ussing chambers (window area
0.28 cm2) equipped with water-jacketed gas lifts,
bathed on both sides with 10 mL of Krebs-Hensleit solution, gassed
with 95% O2 and 5% CO2 and maintained at
37°C. D-Glucose (10 mmol/L) was added to the
serosal-side reservoir and an equimolar amount of mannitol to the
mucosal-side reservoir. The Krebs-Hensleit solution contained
the following (mmol/L): NaCl, 118; KCl, 4.7; NaHCO3, 25;
KH2PO4, 1.2; CaCl2, 2.5;
MgSO4, 1.2; the pH was adjusted to 7.4 after gassing with
5% CO2 and 95% O2. Tissues were
voltage-clamped continuously to zero potential differences by
application of external current, with compensation for fluid
resistance, by means of an automatic voltage current clamp (DVC 1000,
World Precision Instruments, Sarasota, FL). Transepithelial resistance
(
·cm2) was determined by altering the membrane
potential stepwise (± 5 mV) and applying the Ohmic relationship.
Changes in Isc (µA/cm2) were
measured continuously as an index of electrogenic ion transfer. The
voltage/current clamp unit was connected to a PC via a BIOPAC MP1000
data acquisition system (BIOPAC Systems, Goleta, CA). Data analysis was
performed using AcqKnowledge 2.0 software (BIOPAC
Systems).
After a 30- to 45-min preincubation period with vehicle (dimethylsulfoxide, 100 µL) or furosemide (1 mmol/L), by which time the potential difference had stabilized, 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK 14,304) was added to the serosal-side reservoir. Agonist concentration-response curves were constructed in a cumulative manner; each new concentration was added as soon as the potential difference response to the prior concentration reached its nadir.
Na+,K+-ATPase assay.
Na+,K+-ATPase activity in isolated
jejunal epithelial cells was measured by the method of Quigley and Gotterer (1969)
and adapted in our laboratory with slight
modifications. The method of cell isolation was similar to that
described previously (Lucas-Teixeira et al. 2000
).
Isolated epithelial cells were incubated for 15 min at 37°C, and were
then permeabilized by rapid freezing in dry ice/acetone and thawing.
The reaction mixture, in a final volume of 1.025 mL, contained (mmol/L)
37.5 imidazole buffer, 75 NaCl, 5 KCl, 1 sodium EDTA, 5
MgCl2, 6 NaN3, 75
Tris(hydroxymethyl)aminomethane(Tris) hydrochloride and 100
µL cell suspension (100 µg protein).
The reaction was initiated by the addition of 4 mmol/L ATP (25
µL). For determination of ouabain-insensitive
ATPase, NaCl and KCl were omitted, and ouabain (1 mmol/L; 100
µL) or vehicle (water; 100 µL) was
added to the assay. After incubation at 37°C for 20 min, the reaction
was terminated by the addition of 50 µL of
ice-cold trichloroacetic acid. Samples were centrifuged (1500
x g), and liberated inorganic phosphorus
(Pi) in the supernatant was measured by spectrophotometry
at 740 nm. Na+,K+ -ATPase activity is expressed
as nmol Pi/(mg protein · min) and determined as the
difference between total and ouabain-insensitive ATPase. The
protein content in cell suspension (
1.5 g/L), as determined by the
method described by Bradford (1976)
with human serum
albumin as a standard, was similar in all samples.
Radioligand binding.
Membranes from intestinal mucosa were obtained from 20- and
60-d-old rats and prepared according to Nakaki et al. (1983)
. After killing, a segment of jejunum (5–10 cm) was
removed, opened longitudinally along the mesenteric border, rinsed free
from the alimentary contents with cold saline (9 g/L NaCl) and the
jejunal mucosa removed with a scalpel. The jejunal mucosa was
homogenized in 10 mmol/L Tris-HCl, pH 7.4, containing 250 mmol/L
sucrose, 1 mmol/L phenylmethylsulfonyl fluoride, 1 mmol/L EDTA and 5
mg/L each of leupeptin and pesptatin. The cell suspension was
homogenized on ice with a glass-teflon Potter-Elvehjem homogenizer
and then centrifuged at 2600 x g for 15 min at
4°C. The resulting supernatant was centrifuged at 100,000 x g for 60 min at 4°C. The final pellet was resuspended
to a concentration of 1 mg protein/mL in binding buffer (50 mmol/L
Tris-HCl, pH 7.4, at 25°C with 5 mmol/L EDTA). The binding assay
was performed according to Mohuczy-Dominiak and Garg (1993)
with minor modifications. Saturation experiments were
performed in four replicates in 96-well ELISA/RIA plates (Costar
Badhoevedorp, The Netherlands) in a final volume of 0.2 mL
binding buffer containing 0.1–200 nmol/L
[3H]-rauwolscine and 100 µg membrane
protein. Nonspecific binding was determined in the presence of 10
µmol/L phentolamine. After a 45-min incubation at
25°C in a shaking water bath, assays were terminated by vacuum
filtration through glass-fiber filter mats with the Brandel 96-cell
Harvester (Brandel, Gaithersburg, MD). Filters were washed three times
with 200 µL of cold 50 mmol/L Tris-HCl, pH 7.4,
dried and impregnated with MeltiLex A (Wallac, Pharmacia,
Turku, Finland) and radioactivity measured in a Microbeta counter
(model 1450; Wallac).
Drugs.
The compounds used were the following: furosemide and ouabain from Sigma Chemical (St. Louis, Mo); UK 14,304 from Research Biochemicals International (RBI, Natick, MA); and [O-methyl-3H]-rauwolscine (specific activity 2.81 TBq/mmoL) from Nycomed Amersham (Buckinghamshire, U.K.).
Analysis of data.
Half-maximal effective concentration (EC50) values for the
effect of UK 14,304 on Isc, and
Bmax and KD
values for [3H]-rauwolscine saturation curves, were
obtained with nonlinear iterative curve-fitting algorithms using
the GraphPad Prism statistics software package (Motulsky et al. 1994
). Arithmetic means are given with SEM.
Statistical analysis was performed by one-way ANOVA followed by the
Newman-Keuls test for multiple comparisons. A
P-value < 0.05 denoted a significant difference.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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·
cm2 (n = 25) and 51.2 ± 3.2
· m2 (n = 25), respectively. The
effect of 2-adrenoceptor stimulation by UK 14,304
(0.3–3000 nmol/L), applied from the basolateral side, was a
concentration-dependent decrease in Isc
(Fig. 1
), with similar EC50 and maximal effect
(Emax) values in adult fed and food-deprived
rats (Table 1
).
|
|
2-adrenoceptor stimulation in jejunal
preparations from fed and food-deprived rats. The addition of
furosemide (1 mmol/L), a blocker of the NKCC co-transporter
(Frizzell et al. 1979
, Kuo and Shanbour 1980
), to the fluid bathing the serosal side induced a
time-dependent decrease in basal Isc, which
attained its maximum at 20 min and was found to be similar in fed (44
± 11% reduction) and food-deprived (49 ± 12%
reduction) rats. The effect of UK 14,304 on Isc
in both fed and food-deprived rats was significantly attenuated,
but not abolished by furosemide (1 mmol/L) (Fig. 2
).
|
·
cm2 (n = 12) and 50.1 ± 3.8
· cm2 (n = 12),
respectively. As observed in adult rats, the addition of UK 14,304 to
the serosal side (0.3 to 3000 nmol/L) decreased jejunal
Isc in young rats (Fig. 1)
. In contrast to the
observation in adult rats, the Emax in the
20-d-old food-deprived rats was greater than that observed in fed
rats (Fig. 1
and Table 1
). Despite differences in
Emax values for UK 14,304 between fed and
food-deprived rats, no significant differences were observed for
the EC50 values (Table 1)
.
In 20-d-old rats, furosemide was also used during basal and
2-adrenoceptor–stimulated conditions. The
addition of furosemide (1 mmol/L) to the serosal side induced a
time-dependent decrease in basal Isc, which
attained its maximum at 20 min and was found to be similar in fed (48
± 9% reduction) and food-deprived (64 ± 12%
reduction) rats. The effect of UK 14,304 on Isc
in 20-d-old fed rats was completely abolished by furosemide (1 mmol/L)
(Fig. 3
). In 20-d-old food-deprived rats, this effect was also markedly
antagonized by furosemide, but not completely abolished (Fig. 3)
.
|
2-adrenoceptors, the abundance of
2-adrenoceptor binding sites in membranes from
the jejunal mucosa was determined. Figure 4
shows the results of saturation experiments with
[3H]-rauwolscine (0.1–200 nmol/L) performed in
membranes from the jejunal mucosa. Nonlinear analysis revealed the
presence of a single class of binding sites, with an apparent
KD in the low nmol/L range. In
20-d-old food-deprived rats, specific binding of
[3H]-rauwolscine was markedly increased; this
was reversed by refeeding; Bmax and
KD values for
[3H]-rauwolscine specific binding were similar
to those in fed rats (Table 2
).
|
|
). Food deprivation in adult rats was accompanied by a significant
decrease in Na+,K+-ATPase
activity, whereas in 20-d-old rats, food deprivation did not affect
sodium pump activity (Table 3)
. In both young and adult rats (fed and
food-deprived), UK 14,304 did not affect
Na+,K+-ATPase activity
(Table 3)
.
|
|
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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2-adrenoceptors modulate jejunal ion
secretion through modulation of the ionic gradients generated by the
NKCC co-transporter, as evidenced by a furosemide-sensitive UK
14,304–mediated decrease in jejunal Isc.
Moreover, food deprivation in young rats resulted in an enhancement of
the maximal response to UK 14,304 accompanied by an increase in
[3H]-rauwolscine binding. These results raise
the possibility that, in young rats, differences in basal adrenergic
tonus may contribute to changes in intestinal electrolyte transport
during food deprivation.
Multiple transport pathways involved in Na+ and
Cl- transfer are present in the jejunum
(Binder, 1983
, Esposito, 1984
,
Frizzell et al. 1979
). These include transporters,
exchangers, pumps and channels responsible for the electroneutral
absorption of NaCl and electrogenic secretion of
Cl-. In our experimental set-up, a decrease
in basal Isc can be due to a decrease in sodium
absorption, a decrease in chloride or bicarbonate secretion or both
[for details see Vieira-Coelho and Soares-da-Silva (1998)
]. To determine the ionic mechanisms involved in the
2-adrenoceptor–stimulated conditions,
furosemide (1 mmol/L), a NKCC co-transporter inhibitor, was added
to the serosal side of the jejunal epithelium.
In 60-d-old fed rats, basal Isc, which reflects
electrogenic ion movement across the jejunum, was found to be
significantly lower than that in food-deprived rats, suggesting a
more active electrolyte transport in a food-deprived state. Because
food deprivation decreases basal
Na+,K+-ATPase activity,
other pumps or transporters may be responsible for these changes
induced by food deprivation. In fact, food deprivation in adult animals
has been shown to induce changes in the structure of intestinal mucosa,
with a decrease in cell proliferation and a consequent increase in
enterocyte maturity (Johnson 1988
, Williamson 1978
). All of these factors change membrane physical
properties. The decrease in resistance observed in the jejunum of
food-deprived adult rats is in agreement with previous findings by
Young and Levin (1990a)
; these authors found a gradual
decrease in tissue resistance with increasing duration of the fasting
period. Despite differences in basal Isc and
tissue resistance, the addition of UK 14,304 (0.3–3000 nmol/L) to the
serosal side induced a concentration-dependent decrease, with
EC50 and Emax values that
did not differ between fed and food-deprived adult rats. In both
fed and food-deprived rats, the effect of UK 14,304 was partially
antagonized by furosemide, suggesting that the effect of UK 14,304 may
depend in part on the activation of the NKCC co-transporter. The
observation that the
Na+,K+-ATPase activity,
measured in isolated jejunal epithelial cells from fed and
food-deprived rats, was insensitive to UK 14,304 supports the view
that UK 14,304–induced changes in Isc
might depend on the stimulation of the NKCC co-transporter.
In 20-d-old rats, in contrast to adult rats, there were no differences
in basal Isc values between fed and
food-deprived rats. It is possible that 24 h of food
deprivation is not sufficient to change basal electrolyte transport.
Also, no change was observed for tissue resistance. As observed in
adult rats, the addition to the serosal side of UK 14,304 induced a
concentration-dependent decrease in Isc. In
young rats, the response to 2-adrenoceptor
stimulation was markedly potentiated, without changes in
EC50 values. At least two possibilities can be
raised to explain the potentiation in the UK 14,304 response in the
24-h food-deprived young rats. Because EC50
values were not different between fed and food-deprived rats, an
increase in receptor affinity for the agonist can be excluded. Thus,
increases in Emax values for UK 14,304 may result
from either an increase in receptor number, an increase in the number
of transporter units or their sensitivity to modulation by
2-adrenoceptor agonists. Radioligand binding
experiments performed in membranes from the jejunal mucosa from
20-d-old fed and food-deprived rats showed an increase in the
number of binding sites in the membranes of the latter. Refeeding was
accompanied by a reduction in receptor density to a level similar to
that observed in fed rats. Again, to determine the ionic pathways
involved in the UK 14,304 response, furosemide (1 mmol/L) was added to
the serosal side of the intestinal epithelium. In contrast to the
effect observed in adult fed rats, furosemide abolished the UK
14,304–induced decrease in Isc in young fed
rats. However, the inhibitory effect of furosemide on UK
14,304–induced Isc changes was less pronounced
in the jejunum of food-deprived rats. On the other hand, this
difference is consistent with the more pronounced UK 14,304–induced
decrease in Isc in food-deprived rats, which
ultimately may be related to differences in NKCC activity between the
fed and food-deprived rats. The findings that basal
Na+,K+-ATPase activity was
not increased in food-deprived rats and that UK 14,304 did not
alter enzyme activity in either fed or food-deprived rats further
support the hypothesis that NKCC is the major ionic pathway involved in
the response to 2-adrenoceptor activation.
In conclusion, food deprivation in 20-d-old rats enhances the jejunal
electrolyte transport response to
2-adrenoceptor activation. This effect, which
appears to be dependent primarily on the ionic gradients generated by
the NKCC co-transporter mechanism, is likely the result of an
increase in the number of jejunal epithelial
2-adrenoceptors. By contrast, in adult rats,
the response to 2-adrenoceptor stimulation is
not increased by food deprivation despite the differences in basal
Isc, tissue resistance and basal
Na+,K+-ATPase activity.
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FOOTNOTES |
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3 Abbreviations used: EC50, half-maximal effective concentration; Emax, maximal effect; Isc, short-circuit current; NKCC, Na+,K+,2Cl- co-transporter; Pi, free inorganic phosphorus; UK 14,304, 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine.
Manuscript received February 14, 2000. Initial review completed May 16, 2000. Revision accepted July 11, 2000.
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