Postglomerular vasoconstriction induced by dopamine
D3 receptor activation in anesthetized rats
Gerd
Luippold,
Swetlana
Schneider,
Volker
Vallon,
Hartmut
Osswald, and
Bernd
Mühlbauer
Department of Pharmacology, University of Tübingen,
D-72074 Tübingen, Germany
 |
ABSTRACT |
In the present
study we investigated the renal hemodynamic effects of dopamine
D3 receptor activation by
R(+)-7-hydroxy-dipropylaminotetraline (7-OH-DPAT) in
thiopental-anesthetized Sprague-Dawley rats. In clearance experiments
infusion of 7-OH-DPAT (0.01-1.0
µg · kg
1 · min
1)
dose-dependently elevated glomerular filtration rate (GFR) without affecting mean arterial blood pressure (MAP). In renal blood flow experiments 7-OH-DPAT infusion (1.0 µg · kg
1 · min
1)
increased GFR by 16 ± 2%, associated with an unexpected fall in
renal blood flow by 20 ± 3% and a significant elevation of renal
vascular resistance by 18 ± 3%. The renal hemodynamic changes were
not influenced by pretreatment with the D2-receptor
antagonist S(
)-sulpiride but were completely abolished during
D3 receptor inhibition by
5,6-dimethoxy-2-(di-n-propylamino)indane (U-99194A). In micropuncture
experiments 7-OH-DPAT (1.0 µg · kg
1 · min
1)
significantly elevated stop-flow pressure measured in the early proximal tubules and reduced hydrostatic pressure at the first branching point of the efferent arteriole without altering MAP. We
conclude from these data that pharmacological activation of dopamine
D3 receptors affects renal hemodynamics in anesthetized rats by preferential postglomerular vasoconstriction.
R(+)-7-hydroxy-dipropylaminotetraline; 5,6-dimethoxy-2-(di-n-propylamino)indane; S(
)-sulpiride; micropuncture experiments; renal hemodynamics
 |
INTRODUCTION |
DOPAMINE RECEPTORS ARE INVOLVED in the regulation of
cardiovascular and renal function. The five dopamine receptor subtypes identified so far are divided into two subfamilies: the
D1-like receptor, including the D1 and the
D5 receptor, and the D2-like receptor, among
which D2, D3, and D4 receptors are
counted (16). In the rat kidney D1-like receptors were
described, by using polyclonal antisera, in the renal vasculature, the
juxtaglomerular apparatus, the proximal and distal tubule as well as
the cortical collecting duct (3). D2-like receptors have
been suggested, by means of radioligand binding and pharmacological
studies presynaptically on sympathetic nerve terminals in the
adventitia of the renal vasculature and in the glomerulus (5). Very
recently, immunohistochemical studies on the D3 receptor
protein identified this receptor in the proximal and distal tubules,
cortical collecting ducts, glomeruli, and renal arteries (4). Previous
studies on the influence of the dopaminergic system on renal function,
mainly focused on the D1 and D2 receptor
subtypes, revealed conflicting results. Reasons for the discrepant
observations might be differences in species and in type of experiments
in conscious or anesthetized animals. The level of extracellular volume
expansion appears, in addition, to modulate the renal actions of
dopamine (8). Another reason for divergent results may be the
involvement of the other dopamine receptors, i.e., D3,
D4, or D5, the mRNA of which has been
demonstrated in the mammalian kidney (6, 11, 12). Recently, we reported that pharmacological D3 receptor activation with the
selective R(+) enantiomer of 7-hydroxy-dipropylaminotetraline
(7-OH-DPAT) induced a significant diuresis, natriuresis, and an
increase in glomerular filtration rate (GFR) (9). These data prompted
us to elucidate the mechanisms by which D3 receptors might
influence renal hemodynamics. In anesthetized rats, the effects of
7-OH-DPAT on renal hemodynamics were investigated in clearance as well
as renal blood flow (RBF) experiments and micropuncture studies.
 |
METHODS |
Experiments were performed in male Sprague-Dawley rats (Charles River,
Sulzfeld, Germany) weighing 240-280 g. Rats had free access to
standard rat chow (Altromin 1320, Altromin, Lage, Germany) and tap water.
Clearance experiments.
Rats were anesthetized with an intraperitoneal injection of 80 mg/kg thiopental sodium (Byk Gulden, Konstanz, Germany) and placed on a
temperature-controlled heated table (RT, Effenberger, Munich, Germany)
to maintain the body temperature at 37.2°C. After tracheostomy, two
polyethylene (PE) catheters were inserted into the right jugular vein
for intravenous (iv) infusion. The left carotid artery was catheterized
for withdrawal of blood samples and continuous monitoring of blood
pressure (WK 280, WKK, Kaltbrunn, Switzerland). After suprapubic
incision, a PE catheter was placed into the bladder and served for
collection of urine. After the end of preparation the animals were
allowed to reach steady-state conditions, defined by stable systemic
hemodynamics and constant urinary flow rate, which was achieved within
60-90 min. Via the first iv catheter isotonic (0.85%)
saline (NaCl) containing [3H]inulin (1 µCi/ml) was infused at a rate of 0.6 ml/h throughout the entire
experiment for assessment of GFR. Via the second iv catheter NaCl was
infused at a rate of 2.4 ml/h for completion of two baseline clearance
periods. Thereafter, the D3 receptor agonist 7-OH-DPAT
(0.01, 0.03, 0.1, 0.3, 1.0, or 3.0 µg · kg
1 · min
1;
Biotrend, Cologne, Germany) dissolved in NaCl was infused via the
second catheter at the same infusion rate (n = 3-6/dose). Ten minutes after initiation of the 7-OH-DPAT infusion, two
experimental clearance periods were performed. Urine was collected in
20-min periods, and blood samples (180 µl each) were drawn at the
midpoint of each clearance period.
RBF experiments.
Anesthetic procedures and surgery were the same as described in
clearance experiments. The arterial PE catheter was inserted into the
left femoral artery. In addition, after flank incision the hilus of the
left kidney was exposed, and an electromagnetic blood flow transducer
connected to a flowmeter (Carolina Medical Electronics, King) was
fitted around the left renal artery. During careful preparation of the
kidney hilus all visible nerves were left intact. Both the urinary
bladder and the left ureter were cannulated to maintain free urine
flow. After completion of the surgical procedures, the animals were
allowed to stabilize for 90 min before the measurements were started.
[3H]inulin (1 µCi/ml) dissolved in isotonic
NaCl was infused as described above. With the exception of the vehicle
group, this infusion contained either the specific
D3-receptor antagonist 5,6-dimethoxy-2-(di-n-propylamino)indane (U-99194A; 10 µg · kg
1 · min
1;
Research Biochemicals International) or the D2 antagonist
S(
)-sulpiride (SUL; 150 µg · kg
1 · min
1;
Sigma Chemical, Deisenhofen, Germany). Isotonic NaCl was infused via
the second iv catheter at a rate of 2.4 ml/h, and two baseline collection periods were carried out. Thereafter, all groups
(n = 8 each) received 7-OH-DPAT (1 µg · kg
1 · min
1)
dissolved in isotonic NaCl at the same infusion rate. Ten minutes after
onset of the 7-OH-DPAT infusion, two 20-min clearance periods were
performed. Blood samples were drawn at the midpoint of each collection
period, and RBF was determined at the same time.
Micropuncture experiments.
Rats were anesthetized with thiobutabarbital (100 mg/kg ip; Research
Biochemicals International). Surgical preparation was similar to that
described for RBF experiments. Additionally, the left kidney was
exposed, freed of connective tissue, and immobilized in a lucite cup.
The kidney was covered with prewarmed paraffin oil. Both the urinary
bladder and the left ureter were cannulated to maintain free urine
flow. On completion of the surgical preparation, the animals were
allowed to stabilize for 90 min before micropuncture experiments were
started. An estimation of glomerular capillary pressure was assessed by
measuring stop-flow pressure (SFP) in the early proximal tubules. After
identification of nephron configuration, an immobile wax block was
injected into the early proximale tubule. A micropipette (2-3 µm
outer diameter) filled with NaCl (1.5 mol/l) and connected to a
servo-nulling device (World Precision Instruments, New Haven, CT) was
inserted upstream of the wax block to monitor early proximal SFP.
Hydrostatic pressure in the efferent arterioles was assessed by
puncturing the superficial peritubular capillaries at the first
branching point (star vessels). These micropuncture experiments were
carried out in a paired way; i.e., the situation of the tubules and
star vessels was depicted by a drawing, and the same sites were
repunctured during 7-OH-DPAT infusion. In four animals SFP or
hydrostatic pressure in the peritubular capillaries was monitored
continuously before and during 7-OH-DPAT infusion. At baseline, animals
were infused with isotonic (0.85%) NaCl (3.0 ml/h), whereas in the
following experimental period neither NaCl (time controls) nor
7-OH-DPAT (1 µg · kg
1 · min
1)
was infused at the same infusion rate.
Analyses and calculations.
Arterial blood samples were analyzed for hematocrit.
[3H]inulin radioactivity in plasma and urine
was measured by a liquid scintillation counter (2550 TR, Canberra
Packard, Frankfurt, Germany). GFR was determined by the renal clearance
of inulin. Renal vascular resistance (RVR) and filtration fraction (FF)
were calculated according to the standard formula.
Statistical methods.
To evaluate the effects of 7-OH-DPAT on systemic and renal
hemodynamics, the statistical significance of the differences between baseline (NaCl infusion) and experimental periods (7-OH-DPAT infusion) within groups was assessed by the paired two-sided t-test. All values are presented as means ± SE. P values <0.05 were
considered to be statistically significant.
 |
RESULTS |
Clearance experiments.
As shown in Fig. 1 and Table
1, 7-OH-DPAT infusion increased GFR dose
dependently up to a maximum response of 20 ± 2% (ED50 = 0.09 µg · kg
1 · min
1)
whereas mean arterial blood pressure (MAP) was not altered. Heart rate
(HR) remained unchanged by 7-OH-DPAT up to 0.3 µg · kg
1 · min
1
and was slightly but significantly decreased during infusion of 1.0 µg · kg
1 · min
1
(Table 1). Because 3 µg · kg
1 · min
1
of 7-OH-DPAT markedly influenced systemic hemodynamics (Table 1), all
further experiments were performed at 1.0 µg · kg
1 · min
1.

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Fig. 1.
Dose-response curve describing effect of
R(+)-7-hydroxy-dipro-pylaminotetraline (7-OH-DPAT) on glomerular
filtration rate (GFR) in anesthetized rats as percent change from
baseline values (means ± SE; n = 3-6/dose).
Curve was heuristically fitted to a logistic sigmoid equation.
ED50, dose at half-maximal response.
|
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RBF experiments.
In rats of the vehicle group (VHC), 7-OH-DPAT infusion (1.0 µg · kg
1 · min
1)
significantly increased GFR by 16 ± 2% compared with baseline. RBF,
in contrast, was reduced by 20 ± 3% (Fig.
2). These effects were paralleled by a
significant increase in RVR and FF by 18 ± 3 and 36 ± 5%,
respectively (Fig. 3). These changes in
renal hemodynamics were not associated with an alteration in HR or MAP (Table 2). Pretreatment with SUL did not
affect the renal response to 7-OH-DPAT: GFR was significantly elevated
by 18 ± 5%, and RBF was reduced by 22 ± 3%. Thus 7-OH-DPAT
infusion induced an increase in RVR and FF by 19 ± 3 and 40 ± 6%,
respectively (Fig. 3), whereas MAP and HR were not affected during the
entire experiments (Table 2). In contrast to these results,
pretreatment with U-99194A competely abolished the 7-OH-DPAT-induced
renal hemodynamic effects (Figs. 2 and 3). In these experiments,
7-OH-DPAT slightly lowered MAP and HR compared with baseline (Table 2).

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Fig. 2.
Effect of 7-OH-DPAT on GFR (A) and renal blood flow (RBF;
B) dependent on pretreatment with vehicle (VHC),
S( )-sulpiride (SUL) or U-99194A (UAM). Depicted are absolute
values of 7-OH-DPAT infusion (filled bars) compared with baseline
measurement (isotonic saline; open bars). Data are means ± SE and
expressed per 1 kidney; n = 8/group. * P < 0.05 vs. baseline period.
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Fig. 3.
Effect of 7-OH-DPAT on filtration fraction (FF; A) and renal
vascular resistance (RVR; B) dependent on pretreatment with
VHC, SUL, or UAM. Depicted are absolute values of 7-OH-DPAT infusion
(filled bars) compared with baseline measurement (isotonic saline; open
bars). Data are means ± SE and expressed per 1 kidney; n = 8/group. * P < 0.05 vs. baseline period.
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|
Micropuncture experiments.
During baseline, SFP measured in the early proximal tubules (n = 5 rats/8 tubules) as an indicator of glomerular capillary pressure
was 34.8 ± 0.9 mmHg, and hydrostatic pressure in the efferent
arterioles (PE) measured at the first branching point of
the peritubular capillaries (n = 5 rats/8 tubules) was 13.9 ± 0.5 mmHg. In the time control group (n = 4/8), these values were not significantly altered during the entire experiment (Fig. 4). However, intravenous infusion of
7-OH-DPAT (1.0 µg · kg
1 · min
1)
significantly increased SFP (n = 5/8) up to 37.7 ± 0.8 mmHg (P < 0.001) and lowered PE (n = 5 rats/8
tubules) to 12.3 ± 0.4 mmHg (P < 0.003). MAP and HR
remained unchanged during infusion of isotonic saline in the time
control animals, whereas 7-OH-DPAT administration slightly decreased HR
without affecting MAP (Table 3).

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Fig. 4.
Effect of 7-OH-DPAT on stop-flow pressure (SFP; A) in early
proximal tubules and on hydrostatic pressure in efferent arterioles
(PE; B). BAS, baseline period (infusion of isotonic
saline); EXP, experimental period (infusion of isotonic saline in time
controls or 7-OH-DPAT). Data are means ± SE; n = 4 rats, 8 tubules or 8 star vessels in time control rats; n = 5/8/8 in
7-OH-DPAT group. * P < 0.05 vs. baseline period.
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 |
DISCUSSION |
Since the pioneering investigations by Goldberg et al. (for review, see
Ref. 7), numerous functional studies on dopaminergic actions in the
kidney have been carried out, mainly addressing the D1 and
D2 receptor subtypes. However, the experiments revealed unequivocal results. For instance, the D2-like receptor
agonist bromocriptine was reported to increase RBF and single nephron glomerular filtration rate (SNGFR) in anesthetized rats without affecting sodium excretion (21). Similarly, the D2-like
receptor agonist quinpirole was demonstrated to increase SNGFR (15) and whole-kidney GFR in rats (10). In contrast, intrarenal administration of quinpirole in uninephrectomized conscious dogs reduced GFR and renal
plasma flow (18). In a similar study, the D2 antagonist YM-09151 increased GFR, which was paralleled by a significant natriuresis and diuresis (17). These inconsistent observations on renal
effects of dopamine D1 and D2 receptor
activation may be due to differences in species and experimental
settings or to insufficient selectivity of the pharmacological tools
employed. Another reason might be that dopamine receptor subtypes other than D1 and D2 contribute to dopamine-induced
changes in renal function. In this context, D3 receptors
are increasingly gaining interest since Asico et al. (1) suggested that
D3 receptors may play a role in renal and cardiovascular
pathophysiology; transgenic mice lacking both alleles of the
D3 receptor gene developed hypertension combined with an
impaired ability to excrete an acute saline load. The D3
receptor, without doubt, is present in the kidney. Very recently,
O'Connell et al. (4) demonstrated, by light microscopic immunohistochemistry, the localization of this receptor subtype in the
proximal and distal tubules, glomeruli, and renal vasculature. Furthermore, electron microscopic immunocytochemistry revealed D3 receptor staining in the arteriolar smooth muscle cells
of the renal vasculature and on the apical portions of the tubule cells. Pharmacological D3 receptor activation in normal
Sprague-Dawley rats induced an increase in GFR and in urinary volume as
well as sodium excretion (9).
In accordance with the latter observations, in the present experiments
7-OH-DPAT, a selective agonist of D3 receptors (2), increased GFR in a dose-dependent manner (Fig. 1). Arterial blood pressure was not altered, and a slight decrease in HR was observed in
the different experimental groups, irrespective of changes in GFR and
RBF. Therefore, an indirect effect of 7-OH-DPAT on renal hemodynamics,
e.g., by influencing the systemic circulation, appears to be unlikely.
To assess the contribution of D3 receptors to the
7-OH-DPAT-induced renal changes, RBF experiments were performed after
pretreatment with either a D2 or a D3-receptor
antagonist (SUL or U-99194A, respectively). It may be argued that SUL,
as observed in vitro, possessed an only slightly greater
binding affinity for D2 than D3 receptors (19)
and therefore might not discriminate sufficiently between both receptor
subtypes. However, in the present experiments, SUL at a dose sufficient
to inhibit D2 receptors as confirmed previously in vivo
(10) did not alter the renal effects of 7-OH-DPAT whereas inhibition of
D3 receptors by U-99194A (23) completely abolished the
renal effects of 7-OH-DPAT. Taken together, these data indicate that
7-OH-DPAT directly influences renal hemodynamics by selective
activation of D3 receptors in the kidney.
The GFR response to 7-OH-DPAT was accompanied by a reduction in RBF and
an elevated RVR. We hypothesized that this significant increase in FF
might result from vasoconstriction of the postglomerular capillary. In
an attempt to test the hypothesis of a postglomerular vasoconstriction
in response to D3 receptor activation, micropuncture techniques were employed. SFP in early proximal tubules, taken as a
surrogate of glomerular capillary pressure, was significantly increased
by 7-OH-DPAT administration. In accordance with the hypothesis of a
constriction of the efferent arteriole, the hydrostatic pressure in the
first branching point of the efferent arteriole on the kidney surface
was significantly reduced during 7-OH-DPAT infusion. Because a
postglomerular vasoconstriction alone may not be sufficient to explain
a decrease in RBF by 20%, the observed increase in RVR and fall in RBF
in response to 7-OH-DPAT may result from vasoconstriction of both pre-
and postglomerular vessels. The GFR increase despite a fall in RBF
suggests, however, that vasoconstriction prevailed in post- over
preglomerular vessels. The idea that additional factors may come into
play to explain the increase in GFR, e.g., changes in contractile
properties of mesangial cells, has to be addressed in further studies.
A postglomerular vasoconstriction by dopamine D3 receptor
activation has not been described before. Numerous investigations demonstrated that exogenous dopamine, administered in low doses, increases RBF, which was ascribed by most authors to dopamine D1 and, to a lesser extent, to D2 receptor
activation (for review, see Ref. 14). In the split hydronephrotic rat
kidney, Steinhausen et al. (20) observed that locally applied dopamine
dilated both the afferent and, to a lesser extent, the efferent
arterioles; this effect was inhibited by haloperidol, a
dopamine-receptor antagonist with a relatively low selectivity for the
D2 subtype. At higher concentrations, dopamine
also exerted vasoconstrictive effects, but these actions were most
likely due to activation of
-adrenergic receptors. Another
explanation for a 7-OH-DPAT-mediated postglomerular vasoconstriction
might be an indirect effect, e.g., by induction of other vasoactive
mediators such as angiotensin II. However, D3 receptor
activation inhibits renin release from isolated juxtaglomerular cells
(13). Therefore, a D3 receptor-induced release of
angiotensin II appears to be less likely to account for the proposed
efferent arteriolar vasoconstriction in response to 7-OH-DPAT.
In anesthetized rats quinpirole, a D2-like receptor agonist
with a higher in vitro selectivity for D3 over
D2 receptors (19), increased both RBF and GFR (15) whereas
in conscious dogs intrarenal infusion of quinpirole caused a reduction
in both renal parameters (18). These data appear to be rather
inconsistent with the observation of a 7-OH-DPAT-induced
hyperfiltration associated with a decrease in RBF. However, studies on
the selectivity obtained in in vitro assays are not necessarily
applicable to the data in in vivo studies. In addition, quinpirole has
been described to be also a potent agonist at dopamine D4
receptors (22). Recently, the mRNA of this receptor has been
demonstrated in the mammalian kidney (11), but the effects of
D4 receptor activation on renal hemodynamics have not been
investigated so far.
In summary, we demonstrate that D3 receptor activation in
the normotensive anesthetized rat increases RVR asssociated with an
elevation of GFR. Micropuncture experiments supported the hypothesis that an efferent vasoconstriction contributed to this GFR increase. Whether other factors are involved in the 7-OH-DPAT-induced effects on
renal microcirculation has to be clarified by further investigations.
 |
ACKNOWLEDGEMENTS |
We thank Christine Piesch and Kerstin Richter for excellent
technical assistance.
 |
FOOTNOTES |
This study was supported by the Federal Ministry of Education and
Research and the Interdisciplinary Center for Clinical Research (IZKF
Tübingen, 01 KS 9602) and by the Deutsche Forschungsgemeinschaft (Mu 1297/1-2).
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: G. Luippold,
Dept. of Pharmacology, Univ. of Tübingen, Wilhelmstrasse 56, D-72074 Tübingen, Germany (E-mail:
gerd.luippold{at}uni-tuebingen.de).
Received 21 December 1998; accepted in final form 24 November
1999.
 |
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