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
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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
%V<SUB>t change</SUB><IT>=</IT>(<IT>V</IT><SUB>t dep, max</SUB><IT>−V</IT><SUB>t, basal</SUB>)<IT>×100%/V</IT><SUB>t, basal</SUB>

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).

                              
View this table:
[in this window]
[in a new window]
 
Table 1.   Pharmacological profile of dopamine receptors

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
V<SUB>o</SUB><IT>=V</IT><SUB>p</SUB><IT>/t</IT> (1)

J<SUB>Na</SUB><IT>=</IT>(<IT>K</IT><SUB>i</SUB><IT>−K</IT><SUB>o</SUB>)<IT>×V</IT><SUB>o</SUB><IT>/L</IT> (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
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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).


View larger version (15K):
[in this window]
[in a new window]
 
Fig. 1.   Original trace of change in transepithelial voltage (Vt) induced by basolateral dopamine (DA).



View larger version (11K):
[in this window]
[in a new window]
 
Fig. 2.   Dose-dependent change in Vt (%Vt change) in response to basolateral DA (n = 8). P value vs. basal Vt is shown.



View larger version (29K):
[in this window]
[in a new window]
 
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).



View larger version (17K):
[in this window]
[in a new window]
 
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); open circle , 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. dagger P < 0.001 vs. same concentration of basolateral DA alone (by nonpaired t-test). ***P < 0.01 vs. basal (n = 5).

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.


View larger version (20K):
[in this window]
[in a new window]
 
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.



View larger version (14K):
[in this window]
[in a new window]
 
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).

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).


View larger version (14K):
[in this window]
[in a new window]
 
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).

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).


View larger version (15K):
[in this window]
[in a new window]
 
Fig. 8.   Original trace of the Vt change induced by luminal DA.



View larger version (10K):
[in this window]
[in a new window]
 
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.)



View larger version (19K):
[in this window]
[in a new window]
 
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).



View larger version (16K):
[in this window]
[in a new window]
 
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.



View larger version (18K):
[in this window]
[in a new window]
 
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).


View larger version (18K):
[in this window]
[in a new window]
 
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. dagger 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
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

1.   Andersen, PH, and Jansen JA. Dopamine receptor agonists: selectivity and dopamine D1 receptor efficacy. Eur J Pharmacol 188: 335-347, 1990[Medline].

2.   Ando, Y, and Asano Y. Functional evidence for an apical V1 receptor in rabbit cortical collecting duct. Am J Physiol Renal Fluid Electrolyte Physiol 264: F467-F471, 1993[Abstract/Free Full Text].

3.   Ando, Y, and Asano Y. Luminal prostaglandin E2 modulates sodium and water transport in rabbit cortical collecting ducts. Am J Physiol Renal Fluid Electrolyte Physiol 268: F1093-F1101, 1995[Abstract/Free Full Text].

4.   Ando, Y, Breyer MD, and Jacobson HR. Dose-dependent heterogenous actions of vasopressin in rabbit cortical collecting ducts. Am J Physiol Renal Fluid Electrolyte Physiol 256: F556-F562, 1989[Abstract/Free Full Text].

5.   Ando, Y, Tabei K, and Asano Y. Luminal vasopressin modulates transport in the rabbit cortical collecting duct. J Clin Invest 88: 952-959, 1991[ISI][Medline].

6.   Aperia, A. Dopamine action and metabolism in the kidney. Curr Opin Nephrol Hypertens 3: 39-45, 1994[Medline].

7.   Baines, AD, and Chan W. Production of urine free dopamine from DOPA: a micropuncture study. Life Sci 26: 253-259, 1980[ISI][Medline].

8.   Barnett, R, Singhal PC, Scharschmidt LA, and Schlondorff D. Dopamine attenuates the contractile response to angiotensin II in isolated rat glomeruli and cultured mesangial cells. Circ Res 59: 529-533, 1986[Abstract].

9.   Dinerstein, RJ, Vannice J, Henderson RC, Roth LJ, Goldberg LI, and Hoffmann PC. Histofluorescence techniques provide evidence for dopamine-containing neuronal elements in canine kidney. Science 205: 497-499, 1979[ISI][Medline].

10.   Felder, CC, McKelvey AM, Gitler MS, Eisner GM, and Jose PA. Dopamine receptor subtypes in renal brush border and basolateral membranes. Kidney Int 36: 183-193, 1989[ISI][Medline].

11.   Felder, RA, Blecher M, Calcagno PL, and Jose PA. Dopamine receptors in the proximal tubule of the rabbit. Am J Physiol Renal Fluid Electrolyte Physiol 247: F499-F505, 1984[ISI][Medline].

12.   Felder, RA, Felder CC, Eisner GM, and Jose PA. The dopamine receptor in adult and maturing kidney. Am J Physiol Renal Fluid Electrolyte Physiol 257: F315-F327, 1989[Abstract/Free Full Text].

13.   Garcia-Perez, A, and Smith WL. Apical-basolateral membrane asymmetry in canine cortical collecting tubule cells. Bradykinin, arginine vasopressin, prostaglandin E2 interrelationships. J Clin Invest 74: 63-74, 1984[ISI][Medline].

14.   Gingrich, JA, and Caron MG. Recent advances in the molecular biology of dopamine receptors. Annu Rev Neurosci 16: 299-321, 1993[ISI][Medline].

15.   Goldberg, LI, McDonald RH, and Zimmerman AM. Sodium diuresis produced by dopamine in patients with congestive heart failure. N Engl J Med 269: 1060-1064, 1963[ISI].

16.   Jacobson, HR, Gross JB, Kawamura S, Waters JD, and Kokko JP. Electrophysiological study of isolated perfused human collecting ducts: ion dependency of the transepithelial potential difference. J Clin Invest 58: 1233-1239, 1976[ISI][Medline].

17.   Jose, PA, Asico LD, Eisner GM, Pocchiari F, Semeraro C, and Felder RA. Effects of costimulation of dopamine D1- and D2-like receptors on renal function. Am J Physiol Regulatory Integrative Comp Physiol 275: R986-R994, 1998[Abstract/Free Full Text].

18.   Jose, PA, Raymond JR, Bates MD, Aperia A, Felder RA, and Carey RM. The renal dopamine receptors. J Am Soc Nephrol 2: 1265-1278, 1992[Abstract].

19.   Kula, NS, Baldessarini RJ, Kebabian JW, Bakthavachalam V, and Xu L. RBI-257: a highly potent dopamine D4 receptor-selective ligand. Eur J Pharmacol 331: 333-336, 1997[ISI][Medline].

20.   Laduron, PM, and Leysen JE. Domperidone, a specific in vitro dopamine antagonist, devoid of in vivo central dopaminergic activity. Biochem Pharmacol 28: 2161-2165, 1979[ISI][Medline].

21.   Malnic, G, Fernandez R, Cassola AC, Barreto-Chaves ML, de Souza MO, and de Mello-Aires M. Mechanisms and regulation of H+ transport in distal tubule epithelial cells. Wien Klin Wochenschr 109: 429-434, 1997[ISI][Medline].

22.   McDonald, JRH, Goldberg LI, McNay JL, and Tuttle EP, Jr. Effect of dopamine in man: augmentation of sodium excretion, glomerular filtration rate, and renal plasma flow. J Clin Invest 43: 1116-1124, 1964[ISI].

23.   Meister, B, Fryckstedt J, Schalling M, Cortes R, Hokfelt T, Aperia A, Hemmings HJ, Nairn AC, Ehrlich M, and Greengard P. Dopamine- and cAMP-regulated phosphoprotein (DARPP-32) and dopamine DA1 agonist-sensitive Na+,K+- ATPase in renal tubule cells. Proc Natl Acad Sci USA 86: 8068-8072, 1989[Abstract].

24.   Meyer, MB, McNay JL, and Goldberg LI. Effects of dopamine on renal function and hemodynamics in the dog. J Pharmacol Exp Ther 156: 186-192, 1967[ISI][Medline].

25.   Missale, C, Nash SR, Robinson SW, Jaber M, and Caron MG. Dopamine receptors: from structure to function. Physiol Rev 78: 189-225, 1998[Abstract/Free Full Text].

26.   Muto, S, Tabei K, Asano Y, and Imai M. Dopaminergic inhibition of the action of vasopressin on the cortical collecting tubule. Eur J Pharmacol 114: 393-397, 1985[ISI][Medline].

27.   O'Connell, DP, Botkin SJ, Ramos SI, Sibley DR, Ariano MA, Felder RA, and Carey RM. Localization of dopamine D1A receptor protein in rat kidneys. Am J Physiol Renal Fluid Electrolyte Physiol 268: F1185-F1197, 1995[Abstract/Free Full Text].

28.   O'Connell, DP, Vaughan CJ, Aherne AM, Botkin SJ, Wang ZQ, Felder RA, and Carey RM. Expression of the dopamine D3 receptor protein in the rat kidney. Hypertension 32: 886-895, 1998[Abstract/Free Full Text].

29.   Ohbu, K, and Felder RA. D1A dopamine receptors in renal cortical collecting duct. Am J Physiol Renal Fluid Electrolyte Physiol 261: F890-F895, 1991[Abstract/Free Full Text].

30.   Sakairi, Y, Ando Y, Tabei K, Kusano E, and Asano Y. Interleukin-1 inhibits sodium and water transport in rabbit cortical collecting duct. Am J Physiol Renal Fluid Electrolyte Physiol 266: F674-F680, 1994[Abstract/Free Full Text].

31.   Sanada, H, Yao L, Jose PA, Carey RM, and Felder RA. Dopamine D3 receptors in rat juxtaglomerular cells. Clin Exp Hypertens 19: 93-105, 1997[ISI][Medline].

32.   Satoh, T, Cohen HT, and Katz AI. Different mechanisms of renal Na-K-ATPase regulation by protein kinases in proximal and distal nephron. Am J Physiol Renal Fluid Electrolyte Physiol 265: F399-F405, 1993[Abstract/Free Full Text].

33.   Seeman, P, and Van Tol HH. Dopamine receptor pharmacology. Trends Pharmacol Sci 15: 264-270, 1994[ISI][Medline].

34.   Seeman, P, and Van Tol HH. Dopamine receptor pharmacology. Curr Opin Neurol Neurosurg 6: 602-608, 1993[ISI][Medline].

35.   Sibley, DR, and Monsma FJ, Jr. Molecular biology of dopamine receptors. Trends Pharmacol Sci 13: 61-69, 1992[ISI][Medline].

36.   Sibley, DR, Monsma FJ, and Shen Y. Molecular neurobiology of dopaminergic receptors. Int Rev Neurobiol 35: 391-415, 1993[ISI][Medline].

37.   Siragy, HM, Felder RA, Howell NL, Chevalier RL, Peach MJ, and Carey RM. Evidence that intrarenal dopamine acts as a paracrine substance at the renal tubule. Am J Physiol Renal Fluid Electrolyte Physiol 257: F469-F477, 1989[Abstract/Free Full Text].

38.   Sokoloff, P, and Schwartz JC. Novel dopamine receptors half a decade. Trends Pharmacol Sci 16: 270-275, 1995[ISI][Medline].

39.   Sun, D, and Schafer JA. Dopamine inhibits AVP-dependent Na+ transport and water permeability in rat CCD via a D4-like receptor. Am J Physiol Renal Fluid Electrolyte Physiol 271: F391-F400, 1996[Abstract/Free Full Text].

40.   Sun, D, Wilborn TW, and Schafer JA. Dopamine D4 receptor isoform mRNA and protein are expressed in the rat cortical collecting duct. Am J Physiol Renal Physiol 275: F742-F751, 1998[Abstract/Free Full Text].

41.   Suzuki, H, Nakane H, Kawamura M, Yoshizawa M, Takeshita E, and Saruta T. Excretion and metabolism of dopa and dopamine by isolated perfused rat kidney. Am J Physiol Endocrinol Metab 247: E285-E290, 1984[Abstract/Free Full Text].

42.   Takemoto, F, Satoh T, Cohen HT, and Katz AI. Localization of dopamine-1 receptors along the microdissected rat nephron. Pflügers Arch 419: 243-248, 1991[ISI][Medline].

43.   Vermeulen, RJ, Drukarch B, Sahadat MC, Goosen C, Wolters EC, and Stoof JC. The selective dopamine D1 receptor agonist, SKF 81297, stimulates motor behaviour of MPTP-lesioned monkeys. Eur J Pharmacol 235: 143-147, 1993[ISI][Medline].


Am J Physiol Renal Fluid Electrolyte Physiol 281(1):F114-F122
0363-6127/01 $5.00 Copyright © 2001 the American Physiological Society