Departments of 1 Physiology and Biophysics and 2 Anatomy, Instituto de Ciências Biomédicas, University of São Paulo, São Paulo 05508-900, Brazil
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ABSTRACT |
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10.1152/ajprenal.00056.2001. Peritubular arginine vasopressin (AVP)
regulates bicarbonate reabsorption in the cortical distal tubule via
V1 and V2 receptors. The dose-dependent effects
of peritubular AVP on net bicarbonate reabsorption
(JHCO11 M) perfused into peritubular
capillaries increased
JHCO
9 M) also increased
JHCO
11 M) was
significantly higher. A specificV1-receptor antagonist alone or with AVP (10
11 or 10
9 M) reduced
JHCO
11 M) did not affect
JHCO
9 M)-mediated stimulation.
8-Bromoadenosine 3',5'-cyclic monophosphate alone reduced
JHCO
11 M)-mediated
stimulation. (Deamino-Cys1, D-Arg8)
vasopressin (a V2-selective agonist) also reduced
JHCO
arginine vasorpressin; distal bicarbonate reabsorption
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INTRODUCTION |
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THE CORTICAL DISTAL
TUBULE of mammalian kidney plays an important role in the renal
control of H+ secretion and HCO/HCO
channels, play a key role in determining the rate and direction of
bicarbonate transport in this nephron segment (9).
Data from our laboratory showed that luminal arginine vasopressin (AVP;
109 M) stimulates the Na+/H+
exchanger in early distal (ED; distal convoluted tubule) and late
distal (LD; connecting tubule and initial collecting duct) segments, as
well as the vacuolar H+-ATPase in LD segments, via
activation of V1 receptors (3), confirming
previous studies showing that AVP stimulates proton secretion in the
distal tubule (5, 17) and cortical collecting duct
(5, 26). However, the nature of the mechanism underlying AVP action on distal nephron bicarbonate reabsorption is not yet clearly defined because, in A6 cells (an amphibian distal nephron cell
line), the addition of AVP either at low (10
10 M) or at
high (10
6 M) concentrations inhibits the basolateral
Na+/H+ exchanger activity (10).
Besides this, studies in thick ascending limbs showed that AVP
stimulates the basolateral, while inhibiting the apical,
Na+/H+ antiporter (25).
In addition, most studies have detected AVP action when it is applied
at the distal nephron basolateral surface, mediated mostly by
V2 receptors via the adenylate cyclase/cAMP-protein kinase
A signaling system. This pathway, at high-AVP concentrations, is
expected to inhibit the Na+/H+ exchanger
(6). However, in recent years V1 receptors
have been detected in both apical and basolateral membrane domains and
have been shown to mediate AVP activity via phospholipase C-inositol
3,4,5-triphosphate (IP3)-calcium signaling (14, 15, 23). On the other hand, it is known that protein kinase C, via phosphorylation, may stimulate the Na+/H+
exchanger (11). Recently, we have shown that the
stimulatory effect of AVP on the net rate of Na+-dependent
intracellular pH (pHi) recovery in Madin-Darby canine kidney (MDCK) cells, a cell line with many morphological and
physiological similarities to the mammalian distal nephron, is via
activation of V1 receptors located on the basolateral cell
membrane surface and that the basolateral V2 receptors have
a dose-dependent inhibitory effect (22). Thus, with the
consideration that the response of distal bicarbonate reabsorption to
AVP may vary with the hormonal doses being studied and with the type of
receptor present on the distal cell membrane surface, the present study
was designed to determine whether peritubular AVP at either low
(1011 M) or at high (10
9 M) concentrations
regulates bicarbonate transport in the rat cortical distal tubule. For
this purpose, we evaluated the kinetics of HCO
Our results indicate that peritubular AVP stimulates
HCO
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METHODS |
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Male Wistar rats, weighing 200-340 g and obtained from the Instituto de Ciências Biomédicas, were anesthetized with Inactin (100 mg/kg ip; Byk-Gulden, Konstanz, Germany). They received a rat pellet diet and water ad libitum until the time of the experiment. The rats were prepared for in vivo micropuncture as described previously (18). The left jugular vein and left carotid artery were cannulated for infusions and blood withdrawal, respectively. A tracheostomy was performed. The kidney was isolated by a lumbar approach and immobilized in situ by Ringer-agar in a Lucite cup. During the experiment, the rats received venous saline containing 3% mannitol at 0.05 ml/min.
Bicarbonate reabsorption in ED and LD segments was calculated from the continuous measurement of luminal pH by means of microelectrodes in a fluid column isolated by castor oil in the tubule lumen and after the intratubular pH changes toward the steady-state level (12, 18). The microperfusion procedure involved impalement of a proximal loop with a double-barreled micropipette made from theta glass tubing (R&D Optical Systems, Spencerville, MD). One barrel was filled with Sudan black castor oil, and the other was filled with the luminal perfusion solution colored with 0.05% FD&C green. Initially, the luminal perfusion was used to detect ED or LD loops. A double-barreled microeletrode was then inserted into the ED or LD loop. Afterward, luminal perfusion was performed at a rate sufficient to elevate luminal distal tubular loop pH to near that of the original perfusion solution (pH = 8). Then, a column of oil was injected into the proximal tubular lumen, blocking the flow of fluid. Intratubular pH was measured as the voltage difference between the two barrels of the microeletrode made from Hilgenberg (Malsfeld, Germany) double-barreled asymmetric glass capillaries. The larger barrel contained a H+-sensitive ion-exchange resin (Fluka, Buchs, Switzerland), and the smaller one contained 1 M KCl colored by FD&C green (reference barrel). Transepithelial electrical potential difference was the difference between the reference barrel and ground. This parameter was an additional criterion for the recognition of ED or LD segments (13). Intratubular pH changes were recorded continuously in the same tubule with a Beckman model RP dynograph and digitized by a Dell 333D microcomputer equipped with an analog-to-digital conversion board (Lynx, São Paulo, Brazil) for data acquisition and processing.
The luminal pH fell from its initial value of eight toward the
stationary level. Along this curve, intratubular concentrations of
HCO
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The pH microeletrodes were calibrated before and after every impalement on the kidney's surface by superfusion with 20 mM phosphate-Ringer buffer solutions containing 130 mM NaCl at 37°C. The pH values were adjusted to 6.5, 7.0, and 7.5 with 0.1 N NaOH or HCl.
The luminal control perfusion solution contained (in mM) 100 NaCl, 25 NaHCO3, 5 KCl, 1 CaCl2, and 1.2 MgSO4. The osmolality was adjusted to 300 mosmol/kgH2O with raffinose.
In each tubule, several measurements of
JHCO
Peritubular capillaries were perfused with single pipettes made of
thin-walled glass tubes (Kimax; 1.5- to 2.5-mm OD), having a tip
diameter of 10 µm. Air pressure (1-1.2 atm) was applied to these
pipettes for peritubular capillary microperfusion. This perfusion was
considered satisfactory when the perfused area reached two or three
loops beyond the luminally perfused distal segment. Peritubular
capillary perfusion was performed with a solution containing (in mM):
140 NaCl, 20 NaHCO3, 5 KCl, 1 CaCl2, 1.2 MgSO4, and 5 Na+-acetate at pH 7.4. This
solution was preequilibrated with 5% CO2 in air. The
experimental groups of peritubular capillary perfusion solution studied
were selected to combine several possibilities of peritubular drug
administration, i.e., AVP (1011 or 10
9 M)
alone or plus anti-V1 or anti-V2
(10
5 M), 8-Br-cAMP (10
4 M) alone or plus
AVP (10
11 M), and dDAVP (10
9 M). In each
tubule, only one peritubular perfusion solution was used.
AVP (mol wt 1.084), V1-receptor-specific antagonist
[anti-V1; (-mercapto-
,
-cyclopentamethylene-propionyl1, O-Me-Tyr2,
Arg8) vasopressin; (MCMV)] (20),
V2-receptor-specific antagonist [anti-V2,
(adamantaneacetyl1, O-Et-D-Tyr2,
Val4, aminobutyryl6, Arg8,9)
vasopressin] (16, 20), 8-Br-cAMP, dDAVP
[(deamino-Cys1, D-Arg8)
vasopressin], as well as all other applied chemicals were obtained from Sigma, St. Louis, MO.
The pH and PCO2 in samples of blood collected from the carotid artery were measured with a Radiometer ABL 5 blood-gas system. During the experiments, urine flow and Na+ excretion were also measured. Na+ in urine collected from urinary bladder was measured by flame photometry.
The data are shown as means ± SE. Statistical comparisons among parameters of intact, experimental, and postexperimental capillary perfusions performed within the same experimental group were made by using a t-test. Differences among experimental groups were evaluated by analysis of variance (1-way) with contrasts by using the Bonferroni technique, where n is the number of animals (mean of several measurements) when urine or blood collection was performed or the number of perfused tubules (mean of several perfusions).
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RESULTS |
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To detect whether the doses of AVP and V1- or
V2-receptor antagonists used during capillary
microperfusion would cause an effect on renal function and to follow
acid-base conditions of the rats, we measured urine flow,
Na+ excretion, and systemic acid-base parameters. During
capillary microperfusion with these agents, these data were similar to
the basal values found during capillary perfusion with blood [urine flow = 0.147 ± 0.018 ml · min1 · kg
1 (18 measurements, 6 animals); urinary sodium excretion = 8.07 ± 0.85 µeq · min
1 · kg
1 (18 measurements, 6 animals); pH = 7.35 ± 0.12;
PCO2 = 35.3 ± 0.84 Torr and
HCO
In both ED and LD segments, no statistical differences were observed
between the transepithelial electrical potential differences obtained
in all peritubular capillary perfusion groups and the basal values
found during capillary perfusion with blood [ED segments = 16.9 ± 1.58 mV (222 measurements, 93 tubules) and LD
segments =
48.3 ± 4.49 mV (227 measurements, 100 tubules)].
In both ED or LD segments, intratubular steady-state pH values found during capillary microperfusions in all experimental groups were not significantly different from basal data obtained during capillary perfusion with blood [ED segments = 6.99 ± 0.55 (n = 222 measurements and 93 tubules) and LD segments = 7.05 ± 0.63 (n = 227 measurements and 100 tubules)], indicating that during peritubular capillary perfusion with an artificial solution at physiological pH and PCO2, tubular acidifying capacity was maintained at normal levels.
The mean half-time of the reduction in luminally injected
HCO
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Figure 1 shows the sequence of perfusion
in four different ED segments to which the control solution or AVP
(1011 M) was applied during peritubular capillary
perfusion. During capillary perfusion with the control solution, it is
apparent that over a period of several minutes no significant change in bicarbonate reabsorption occurs compared with basal levels during intact capillary perfusion with blood (Fig. 1A), confirming
the capacity of the distal tubule to maintain an adequate rate of acidification during capillary perfusion with an artificial solution at
physiological pH and PCO2. It is clear that AVP
(10
11 M) added to the capillary solution significantly
stimulates HCO
11 M)-mediated stimulation below basal blood perfusion
levels (Fig. 1C). These data indicate that endogenous AVP
stimulates distal bicarbonate reabsorption via V1 receptors
and that the capillary administration of AVP (10
11 M)
increases this process. However, the addition of anti-V2
does not affect AVP (10
11 M)-mediated stimulation (Fig.
1D). It is also clear that, in all of these situations,
recovery of basal levels occurs after the experimental capillary
perfusion. Figures 2 and
3 give mean data of bicarbonate
reabsorption in ED and LD segments to which these experimental
solutions were applied in the capillary perfusion.
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Figure 4 shows that the capillary
administration of AVP (109 M) also increases ED and LD
HCO
9 M)-mediated HCO
9 M) is given together with anti-V2, the
effect on bicarbonate reabsorption is significantly greater than with
AVP (10
9 M) alone in ED and LD segments, indicating that
V2 receptors have a dose-dependent inhibitory effect. Also,
in these situations, recovery of basal levels is observed after the
experimental capillary perfusions.
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Figure 5 gives the effect of the addition
of 8-BrcAMP (104 M; a membrane-permeant cAMP analog) to
the experimental peritubular capillary perfusion in ED and LD segments.
8-BrcAMP alone reduces JHCO
11
M)-mediated stimulation, showing an inhibitory effect mediated by cAMP.
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Figure 6 summarizes the previous results
obtained in ED and LD segments. The effect of 1011 M AVP
was higher than that of 10
9 M AVP. However, when
anti-V2 is given together with 10
9 M AVP,
bicarbonate reabsorption increases toward the 10
11
M AVP values. On the other hand, in the presence of 8-BrcAMP the effect
of 10
11 M AVP is similar to the effect of
10
9 M AVP alone. These results indicate that the
stimulation of V2 receptors has a dose-dependent inhibitory
effect mediated by cAMP.
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Confirming this hypothesis, Fig. 7 shows
that dDAVP (109 M; an AVP analog that specifically binds
to adenylyl cyclase-coupled V2 receptors) reduces
HCO
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DISCUSSION |
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The cortical distal tubule of the mammalian kidney has an
important role in the renal control of H+ secretion and
HCO11 or
10
9 M) on the kinetics of HCO
In all groups studied, in ED and LD segments during the recovery period
after experimental capillary perfusion, a recovery of basal levels of
the bicarbonate reabsorption was observed, indicating that the
substitution of peritubular capillary blood by artificial solutions
appears to be a valid method for the study of factors affecting tubular
acidification. Furthermore, repeated luminal perfusion procedures did
not significantly alter the transepithelial electrical potential
difference, intratubular steady-state pH values, and
JHCO
In addition, no significant differences were observed between
intratubular steady-state pH values of capillary-perfused groups and
the respective control groups. Changes in this parameter are related to
several factors, including the function of H+ and
HCO
Our results indicate that peritubular AVP (1011 or
10
9 M) has a direct effect, stimulating
HCO
Our results show that the addition of anti-V1 to
peritubular perfusion reduces AVP (1011 or
10
9 M)-mediated HCO
At high concentrations, AVP is known to interact with V1
receptors, causing the liberation of arachidonic acid, which is part of
a path that elevates cell calcium and, consequently, may inhibit the
Na+/H+ exchanger (24). This
inhibitory effect of a high concentration of AVP via V1
stimulation is apparent in our present data in ED and LD segments,
which show that the stimulatory effect of peritubular 1011 M AVP plus anti-V2 on distal bicarbonate
reabsorption is higher than with 10
9 M AVP plus
anti-V2 (Fig. 6).
It is well known that V2 receptors mediate a dose-dependent
adenylate cyclase-cAMP-protein kinase A pathway that, at high-AVP concentrations, is expected to inhibit the
Na+/H+ exchanger (6). This
behavior is compatible with our present data in ED and LD segments,
showing that a V2-receptor antagonist plus
1011 M AVP does not affect
JHCO
9 M AVP increases
JHCO
11 M AVP alone is given (Fig.
6). These data indicate that, in presence of 10
11 M AVP,
the cAMP levels are too low to inhibit the
Na+/H+ exchanger. These results also show that
the inhibitory effect of a high concentration of AVP was prevented by
simultaneous capillary perfusion with the anti-V2 agent. In
addition, our present results show that with 8-BrcAMP (a cAMP analog)
the effect of 10
11 M AVP is similar to the effect of
10
9 M AVP alone (Fig. 6), confirming that in presence of
10
11 M AVP alone the cAMP levels are too low to inhibit
the Na+/H+ exchanger. These data also indicate
that V2 receptors have a dose-dependent inhibitory effect
mediated by cAMP. This hypothesis is confirmed by our results showing
that dDAVP (an AVP analog that specifically binds to adenylyl
cyclase-coupled V2 receptors) reduces
HCO
9 M luminal AVP stimulates the
Na+/H+ exchanger and H+-ATPase in
the cortical distal tubule via luminal V1 receptors (3). Our present results also show that the presence of
the V2-receptor antagonist alone in peritubular perfusion
has no effect on bicarbonate reabsorption in ED and LD segments (Fig.
2). These results indicate that in basal conditions the basolateral
V2 receptors are not stimulated, confirming that these
receptors have a hormonal dose-dependent inhibitory effect. This dual
regulation of bicarbonate reabsorption may represent a relevant
regulatory mechanism that prevents blood alkalinization in conditions
of volume depletion, because it is known that plasma AVP usually
reaches levels 20-30 times greater than normal when blood volume
is reduced by 20-30% (in rats, dogs, and humans) or plasma
osmolality is increased by 10% (4).
The effect of AVP during peritubular capillary perfusion raises the question of the distribution of receptors for this peptide on the cell surface. It appears reasonable to believe that the effect of AVP during capillary perfusion occurs due to the presence of V1 and V2 receptors at the distal cell basolateral membrane surface, because it is improbable that in tight epithelia such as the distal tubule this peptide could reach the luminal membrane via the paracellular shunt path during peritubular perfusion. In addition, our present data confirm earlier findings showing that, in rabbit cortical collecting duct, electrical responses to AVP in the bath are a composite of basolateral V1 and V2 receptor-mediated actions (29).
The possible physiological role of peritubular AVP action should also
be considered. Our results show that the addition of V1-receptor antagonist alone or with 1011 or
10
9 M AVP to peritubular capillary perfusion reduces
bicarbonate reabsorption in ED and LD segments below the levels found
during blood capillary perfusion (Figs. 1-4). This could be due to
an unspecific inhibitory action of this V1-receptor
antagonist, but it might also indicate that, in basal conditions, a
basal level of AVP binding to peritubular V1 receptors may
exist, causing some tonic activation of bicarbonate reabsorption.
Inhibitory action of this nature has been reported before by Amorim and
Malnic (1), demonstrating that the
V1-antagonist MCMV (the same used by us in the present experiments) reduces distal K+ secretion in Wistar rats
when given alone. To eliminate the possibility of an unspecific
inhibitory effect of the V1-antagonist MCMV, these authors
performed experiments in homozygous Brattleboro rats [which are known
to be devoid of endogenous AVP production (27)], showing
that this anti-V1 agent had no AVP-independent action,
despite the presence of AVP receptors in these rats. On the basis of
these findings, we may conclude that in basal conditions endogenous AVP
stimulates bicarbonate reabsorption in ED and LD segments. On the other
hand, our data show that there was no difference between the
bicarbonate reabsorption of the basal group (in presence of intact
capillary perfusion with blood) and the control solution capillary
perfusion group (Fig. 2), which is apparently incompatible with the
concept of endogenous AVP-stimulated bicarbonate reabsorption. However,
an additional question involves the duration of AVP binding to its
receptors in distal tubule basolateral membranes. Figure 1B
indicates that AVP washout (during the recovery period in presence of
capillary perfusion with blood) is not immediate but that it takes
several minutes for levels to approach preexperimental capillary perfusion basal levels (during intact capillary perfusion with blood),
suggesting that the maintenance of residual levels of AVP binding in
basal conditions might be expected in the presence of capillary
perfusion with a control solution. In addition, Figs. 1A and
2 demonstrate that, during capillary perfusion with the control
solution, bicarbonate reabsorption does decrease somewhat but not
significantly. Taken together, these findings support the view
that, in basal conditions, a portion of normally observed distal
bicarbonate reabsorption may be dependent on endogenous AVP levels.
In conclusion, we have undertaken in vivo stationary microperfusion
studies in ED and LD segments of rat cortical tubule to evaluate the
effects of peritubular capillary AVP (1011 and
10
9 M) on HCO
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ACKNOWLEDGEMENTS |
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We thank Dr. Gerhard Malnic, University of São Paulo, Brazil, for a careful reading of the manuscript and for helpful suggestions.
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FOOTNOTES |
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This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq-PADCT and Pronex). Portions of this work were presented at the Annual Meeting of the American Society of Nephrology, Toronto, Ontario, Canada, October 2000, and were published in abstract form (J Am Soc Nephrol 11: A0034, 2000).
Address for reprint requests and other correspondence: M. de Mello-Aires, Dept. of Physiology and Biophysics, Instituto de Ciências Biomédicas, Univ. of São Paulo, Av. Professor Lineu Prestes, 1524, SP 05508-900, Brazil (E-mail: mmaires{at}fisio.icb.usp.br).
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.
10.1152/ajprenal.00056.2001
Received 20 February 2001; accepted in final form 29 September 2001.
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