Published online before print February 7, 2005, doi: 10.1161/01.HYP.0000155212.33212.99
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(Hypertension. 2005;45:804.)
© 2005 American Heart Association, Inc.
Original Articles |
Interaction of Angiotensin II Type 1 and D5 Dopamine Receptors in Renal Proximal Tubule Cells
From the Department of Cardiology (C.Z.), Daping Hospital, Third Military Medical University, Chongqing, P.R. China; Departments of Pediatrics (Z.Y., Z.W., J.J., X.W., J.A., P.A.J.), Physiology and Biophysics (Z.Y., P.A.J.), and Medicine (G.M.E.), Georgetown University Medical Center, Washington, DC; Departments of Medicine (A.J.M.) and Pathology (R.A.F.), University of Virginia Health Sciences Center, Charlottesville; Department of Physiology and Biophysics (U.H.), Case Western Reserve School of Medicine, Cleveland, Ohio; and Molecular Neuropharmacology Section (D.R.S.), National Institute of Neurological Disorders and Stroke/NIH, Bethesda, Md.
Correspondence to Dr Chunyu Zeng, Department of Pediatrics, PHC-2, Georgetown University Medical Center, 3800 Reservoir Rd NW, Washington, DC 20007. E-mail cyzeng1{at}hotmail.com
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Abstract |
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Angiotensin II type 1 (AT1) receptor and D1 and D3 dopamine receptors directly interact in renal proximal tubule (RPT) cells from normotensive Wistar-Kyoto rats (WKY). There is indirect evidence for a D5 and AT1 receptor interaction in WKY and spontaneously hypertensive rats (SHR). Therefore, we sought direct evidence of an interaction between AT1 and D5 receptors in RPT cells. D5 and AT1 receptors colocalized in WKY cells. Angiotensin II decreased D5 receptors in WKY cells in a time- and concentration-dependent manner (EC50=2.7x10–9 M; t1/2=4.9 hours), effects that were blocked by an AT1 receptor antagonist (losartan). In SHR, angiotensin II (10–8 M/24 hours) also decreased D5 receptors (0.96±0.08 versus 0.72±0.08; n=12) and to the same degree as in WKY cells (1.44±0.07 versus 0.92±0.08). However, basal D5 receptors were decreased in SHR RPT cells (SHR 0.96±0.08; WKY 1.44±0.07; n=12 per strain; P<0.05) and renal brush border membranes of SHR compared with WKY (SHR 0.54±0.16 versus WKY 1.46±0.10; n=5 per strain; P<0.05). Angiotensin II decreased AT1 receptor expression in WKY (1.00±0.04 versus 0.72±0.08; n=8; P<0.05) but increased it in SHR (0.96±0.04 versus 1.32±0.08; n=8; P<0.05). AT1 and D5 receptors also interacted in vivo; renal D5 receptor protein was higher in mice lacking the AT1A receptor (AT1A–/–; 1.61±0.31; n=6) than in wild-type littermates used as controls (AT1A+/+; 0.81±0.08; n=6; P<0.05), and renal cortical AT1 receptor protein was higher in D5 receptor null mice than in wild-type littermates (1.18±0.08 versus 0.84±0.07; n=4; P<0.05). We conclude that D5 and AT1 receptors interact with each other. Altered interactions between AT1 and dopamine receptors may play a role in the pathogenesis of hypertension.
Key Words: receptors, dopamine • receptors, angiotensin II • rats, spontaneously hypertensive • normotension • kidney
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Introduction |
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Several cardiovascular diseases, including hypertension, are associated with abnormal regulation of sodium balance. This balance is regulated by natriuretic and antinatriuretic hormones and humoral agents.1–8 Among the numerous factors involved in this process are angiotensin II and dopamine. During moderate volume expansion, renal dopamine production is increased, and dopamine, via D1-like (comprised of D1 and D5 subtypes) and D2-like receptors (comprised of D2, D3, and D4 subtypes), acts to increase sodium excretion.1,5–8 In contrast, during salt deprivation, angiotensin II production is increased, and angiotensin II, via angiotensin II type 1 (AT1) receptors, increases renal sodium transport.2–4 Angiotensin II antagonizes the natriuretic response elicited by dopamine, and dopamine opposes angiotensin II–mediated sodium transport in the renal proximal tubules (RPTs).9,10 Even a small increase in intracellular sodium concentration induces an increase in D1 receptors and a decrease in AT1 receptors in renal cell surface membranes.11 Although the counter-regulation between dopamine and angiotensin II receptors has been shown primarily in RPTs, these receptors may also interact in other areas in the kidney.5,11–13
In addition to counter-regulation of sodium transport by D1-like and AT1 receptors in RPT cells, they also each interact to regulate expression of the other.14–19 AT1, D1, and D3 receptors may interact, directly or indirectly, in RPT cells from normotensive Wistar-Kyoto rats (WKY).15–19 Activation of D1-like or D3 receptors decreases AT1 receptor expression in RPT cells from WKY.15,17 A physical interaction between the other D1-like receptor (ie, D5) and the AT1 receptor has not been reported, although there is indirect evidence for a negative interaction between D5 and AT1 receptors in RPT cells.15 In that study, we found that a D1-like receptor, presumably the D5 receptor, was capable of decreasing AT1 receptor expression in RPT cells from WKY and spontaneously hypertensive rats (SHR). Therefore, we sought direct evidence of an interaction between the AT1 receptor and the D5 receptor in RPT cells and determined whether this interaction is different between WKY and SHR.
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Methods |
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AT1A Receptor–Deficient Mice
The characteristics and genotyping of mice lacking the AT1A receptor (AT1A–/–) have been reported.2,20,21 The current studies used second-generation AT1A–/– mice from first-generation heterozygous mice of mixed C57BL/6 and B129 background from the University of Virginia. Gender-matched, wild-type littermates were used as controls (AT1A+/+). After mice were anesthetized with CO2, kidneys were harvested, snap-frozen in liquid nitrogen, stored at –70°C, and shipped to Georgetown University Medical Center.
Generation of Mice Lacking the D5 Receptor
The generation of mice lacking the D5 receptor (D5–/–) has been reported.22,23 These mice developed hypertension after 2 months of age.23 The current studies used D5–/– mice generated in a C57BL/6 Taconic background. Gender-matched, nontransgenic littermates were used as controls (D5+/+).
Blood Pressure Studies
The rats (Taconic; Germantown, NY) were anesthetized with pentobarbital (50 mg/kg IP) and placed on a heated board to maintain body temperature at 37°C. Catheters were inserted into the femoral vessels and right jugular vein. After stable blood pressures were obtained for 
30 minutes (verifying that the SHR were hypertensive and the WKY were normotensive), kidneys were removed and the rats euthanized (pentobarbital; 100 mg/kg IV). The renal cortices were homogenized in ice-cold lysis buffer (PBS with 1% Nonidet P-40, 0.5% sodium deoxycholate, 0.1% sodium dodecyl sulfate, 1 mmol/L EDTA, 1 mmol/L EGTA, 1 mmol/L PMSF, 10 µg/mL aprotinin, and 10 µg/mL leupeptin), sonicated, kept on ice for 1 hour, and centrifuged at 16 000g for 30 minutes. The supernatants were stored at –70°C until use for immunoblotting.15–19,24–27 All experiments were approved by the Georgetown University animal use and care committee.
Cell Culture
Immortalized RPT cells obtained from 4- to 8-week-old WKY and SHR were cultured at 37°C in 95% air/5% CO2 atmosphere in DMEM/F-12 culture media.15–18,25–27 These RPT cells have characteristics similar to freshly obtained RPT brush border membranes and RPTs, at least with regard to D1 receptors and responses to G-protein stimulation.25–27 The cells (80% confluence) were extracted in ice-cold lysis buffer, sonicated, kept on ice for 1 hour, and centrifuged at 16 000g for 30 minutes. The supernatants were stored at –70°C until use for immunoblotting.
Immunoblotting
AT1 receptor antibody (Abcam Limited) is a mouse monoclonal antibody; the specificity of this antibody to the AT1 receptor has been reported.28 The amino acid sequence of the peptide for the rabbit anti-human D5 receptor antibody corresponds to the third intracellular loop of the D5 receptor. We reported the specificity of this D5 receptor antibody.29 Rat RPT cells were treated with vehicle (distilled H2O), angiotensin II (Peninsula Laboratories) or an AT1 receptor antagonist (losartan; Merck) at the indicated concentrations and times.30 Immunoblotting was performed as reported previously, except that the transblots were probed with the D5 (1:500) or the AT1 receptor antibody (1:400).15–19,24–27,29
The blots were scanned and the densities expressed as percent area, with the total area in a particular group set at 100%.15–18,24–27,29 When appropriate, the densities of the receptor bands were corrected by the density of the 
-actin band.
Confocal Microscopy of Double-Stained RPT Cells
RPT cells, grown on coverslips, were fixed and permeabilized with 100% methanol (30 minutes). The D5 receptor was visualized using a rabbit anti-human D5 receptor antibody followed by a fluorescein isothiocyanate (FITC)–conjugated anti-rabbit secondary antibody (Molecular Probes) or by a mouse anti-AT1 receptor monoclonal antibody (Abcam Limited), followed by an Alexa Fluor 568–goat anti-mouse IgG antibody (Molecular Probes). Cells on coverslips were mounted with the ProLong Antifade Kit (Molecular Probes). Negative controls included absence of primary or secondary antibodies. Immunofluorescence densities and images were acquired (Olympus AX70) at an excitation wavelength of 488 and 568 nm; emission was detected at 535 and 645 nm.29
Statistical Analysis
Data are expressed as mean±SEM. Comparison within groups was made by ANOVA for repeated measures (or paired t test when only 2 groups were compared), and comparison among groups (or t test when only 2 groups were compared) was made by ANOVA with Holm–Sidak test. A value of P<0.05 was considered significant.
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Results |
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AT1 Receptors Decrease D5 Receptor Expression in RPT Cells From SHR and WKY
Angiotensin II decreased D5 receptors in a concentration- and time-dependent manner in RPT cells from WKY. The maximum inhibitory effect was 43%; it was significant at and >10–8 M; the concentration for half-maximal inhibition was 2.7x10–9 M (Figure 1A). The inhibitory effect of angiotensin II (10–8 M) was noted as early as 8 hours and maintained for
30 hours (t1/2=4.9 hours; Figure 1B).
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The specificity of angiotensin II as an AT1 receptor agonist was also determined by studying the effect of the AT1 receptor antagonist losartan. Consistent with the study shown in Figure 1A and 1B, angiotensin II (10–8 M/24 hours), decreased D5 receptors in WKY cells (control 1.10±0.06; angiotensin II 0.76±0.06; n=7; P<0.05). The AT1 receptor antagonist losartan (10–8 M/24 hours), by itself, had no effect on D5 receptor expression (1.04±0.06) but reversed the inhibitory effect of angiotensin II on D5 receptor expression (1.10±0.06; Figure 1C).
We next compared the effect of angiotensin II on D5 receptor expression studied concurrently in RPT cells from WKY and SHR. In RPT cells from WKY and SHR, angiotensin II (10–8 M/24 hours) also decreased D5 expression (WKY 1.44±0.07 versus 0.92±0.08; SHR 0.96±0.08 versus 0.72±0.08; n=12), and the degree of reduction in SHR (28±7%) was similar to that noted in WKY cells (35±6%; Figure 1D).
Basal D5 receptor levels were lower in SHR than in WKY RPT cells (0.96±0.08 versus 1.44±0.07; n=12; Figure 1D). D5 receptor protein was also decreased in brush border membranes from the kidney of SHR compared with WKY (WKY 1.46±0.16 versus SHR 0.54±0.10; n=5; P<0.01; Figure 1E).
Angiotensin II Decreases AT1 Receptor Expression in RPT Cells From WKY But Increases It in SHR
To confirm our previous report on the effect of angiotensin II on AT1 receptor expression in RPT cells,16 we used a different monoclonal AT1 antibody in this study. RPT cells were incubated with angiotensin II for the indicated times and concentrations. Angiotensin II decreased AT1 receptor expression in a concentration- and time-dependent manner in RPT cells from WKY (EC50=6.6x10–8 M; t1/2=4.2 hours; Figure 2A and 2B). Whereas angiotensin II decreased its own receptor expression in RPT cells from WKY, it increased it in RPT cells from SHR (WKY 1.00±0.04 versus 0.72±0.08; SHR 0.96±0.04 versus 1.32±0.08; n=8; P<0.05; Figure 2C), in agreement with our previous report.16
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AT1 Receptor Colocalizes With the D5 Receptor in Rat RPT Cells
To determine the potential for a direct or indirect interaction between D5 and AT1 receptors, we studied the colocalization of D5 and AT1 receptors in RPT cells from WKY. D5 and AT1 receptors were found throughout the cell, with evidence of colocalization, especially at the cell surface membrane (Figure 3). To determine whether there is a physical interaction between the D5 and the AT1 receptor, additional experiments were performed. D5 receptors were first immunoprecipitated with anti-D5 receptor antibodies and the immunoprecipitate analyzed by immunoblotting with anti-AT1 receptor antibodies. Additionally, antibodies were reversed for immunoprecipitation and immunoblotting. No D5/AT1 receptor coimmunoprecipitation bands were found (data not shown).
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D5 Receptor Expression Is Increased in the Kidneys of AT1–/– Mice
Although the coimmunoprecipitation study showed no evidence for a direct physical interaction between AT1 and D5 receptors, we determined whether the AT1 receptor could regulate D5 receptor expression in vivo. The D5 and AT1 receptors each can regulate expression of the other because D5 receptor protein expression was greater in kidneys of AT1–/– (1.61±0.31; n=6) than AT1+/+ littermates (0.81±0.08; n=6; P<0.05; Figure 4).
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AT1 Receptor Expression Is Increased in the Kidneys of D5–/– Mice
We next determined whether the D5 receptor could regulate AT1 receptor expression in vivo. We found that F6 pentobarbital-anesthetized congenic D5–/– mice (F6) had higher systolic blood pressure (SBP) and diastolic blood pressure (DBP; SBP 117±5 mm Hg; DBP 85±2 mm Hg; n=5) than wild-type C57BL/6 (Taconic) mice (SBP 94±2 mm Hg; DBP 69±3 mm Hg; n=5; P<0.05; t test), in agreement with previous reports.23,31 The arterial blood pressures of awake D5–/– mice were in the hypertensive range.23,31 Immunoreactive AT1 receptors were also greater in the kidney of D5–/– than D5+/+ littermates (D5–/– 1.18±0.08; D5+/+ 0.84±0.07; n=4; P<0.05; Figure 5).
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Discussion |
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Alterations in the responsiveness of the proximal tubule to angiotensin II and dopamine have important implications for net sodium reabsorption. Several studies have shown that the dopaminergic and renin-angiotensin systems interact to regulate renal function.9–11,15,16 For example, inhibition of renal angiotensin II production or blockade of AT1 receptors increases the natriuretic effect of the D1-like agonist fenoldopam.9,32 D1-like and D2-like receptor agonists also antagonize the stimulatory effect of angiotensin II, acting via AT1 receptors, on renal proximal tubular luminal sodium transport.10,33,34 The renal vasoconstrictor effect of angiotensin II can also be antagonized by D1-like receptor agonists,35 and angiotensin-converting enzyme inhibition augments the renal vasodilator effect of a D1-like receptor agonist.36 Our previous studies showed that dopamine, via D1-like and D3 receptors, inhibits AT1 receptor expression;15,17 indirect evidence suggests that the D5 receptor may be involved in the inhibitory effects of a D1-like receptor on AT1 receptor.15 This is consistent with our finding in human RPT cells indicating that the D5 but not the D1 receptor decreases AT1 receptor expression,37 and AT1 receptor expression in renal cortical membrane of D5–/– mice is increased relative to wild-type littermates.
To better understand the interaction between dopamine and AT1 receptors, we investigated the effect of AT1 receptor activation on the expression of dopamine receptor subtypes in RPT cells. In a preliminary communication, we reported that activation of the AT1 receptor increases D1 receptor expression in RPT cells from WKY but not from SHR.18
The ability of dopamine and D1-like agonists to couple to signal transducers and decrease renal proximal tubular sodium reabsorption is impaired in genetic rodent hypertension and human essential hypertension.1,5,7,8,26,38 Indeed, the aberrant D1-like receptor function in the kidney precedes and cosegregates with high blood pressure in SHR.1,5,7,8 In addition, disruption of the D1 or D5 receptor in mice produces hypertension.23,31,39 Although total cellular D1 receptor expression is not different in RPT cells of WKY and SHR, D1-like receptor-mediated natriuresis is impaired in SHR because of an uncoupling of D1-like receptors from their G-protein/effector enzyme complex.1,5,7,8,26 In this study, we find that D5 receptor expression is decreased in RPT cell and renal brush border membranes from SHR compared with WKY cells. Because the increase in cAMP levels after D1-like receptor stimulation is attributable mainly to the D1 receptor relative to the D5 receptor,40 we speculate that the effect of AT1 receptors on D5 receptor expression may not have as significant an impact on renal tubular function relative to the effect of the AT1 receptor on the D1 receptor. However, the ability of the D5 receptor to negatively regulate the AT1 receptor may have a significant impact on the regulation of blood pressure. Indeed, in the current report, we show that renal D5 receptor protein is increased in AT1A receptor–deficient mice, and renal AT1 receptor is increased in D5 receptor–deficient mice, relative to their wild-type littermates.
The role of this differential expression of D5 receptors on renal sodium handling remains to be determined. However, the hypertension in D5–/– mice is aggravated by increased sodium intake.41 We speculate that this may be, in part, attributable to increased renal expression of AT1 receptors. We have preliminary studies showing that the intraperitoneal administration of the AT1 receptor antagonist losartan (20 mg/kg per day for 8 days) normalized blood pressure in pentobarbital D5–/– mice but minimally affected blood pressure in D5 +/+ littermates (L.D. Asico et al, unpublished data, 2004). The decreased expression of D5 receptors in SHR and the increased expression of AT1 receptors in D5–/– mice may be a mechanism of the unmitigated AT1 receptor function in hypertension.
The mechanism for the decrease in D5 receptor caused by AT1 receptors was not studied. We find colocalization of D5 and AT1 receptors in RPT cells. However, there is no physical interaction determined by coimmunoprecipitation study, which indicates that D5 and AT1 receptors interact with each other via an indirect pathway. We have reported in a preliminary communication that the D5 receptor decreases AT1 receptor expression by increasing its degradation in human RPT cells.37 It is possible that the AT1 receptor regulates D5 receptor expression by similar mechanisms.
The effect of angiotensin II on AT1 receptor expression in RPT cells has not been consistent. In rabbit RPT cells, a 16-hour incubation with angiotensin II dose-dependently increases AT1 receptor expression, assessed by radioligand binding.42 AT1 receptor mRNAs in rat and rabbit RPT cells are also increased by angiotensin II.43,44 However, the intravenous administration of angiotensin II that increases systemic blood pressure does not alter immunoreactive renal AT1 receptor expression but decreases AT1 receptor expression (radioligand autoradiography) in glomeruli and inner stripe of the outer medulla. Three days after the infusion of angiotensin II, there is a tendency for a decrease in AT1 expression in the whole kidney and in RPTs, but the changes are modest and do not reach statistical significance.44 We reported that angiotensin II decreases AT1 receptor, determined by immunoblotting, in cells from WKY.16 Because the specificity of commercially available antibodies has been questioned, the current studies used a different AT1 receptor antibody. Using a monoclonal AT1 receptor antibody, we again find that angiotensin II decreases AT1 expression in RPT cells from WKY but produces the opposite effect in SHR. This contrasting effect of angiotensin II on AT1 receptor expression in WKY and SHR suggests that our findings cannot be explained by limitations of AT1 receptor antibodies. Rather, the strain-specific effect of angiotensin II on AT1 receptor may be important in the pathogenesis of hypertension in SHR. However, it is realized that the renal expression of AT1 receptors in SHR has not been consistently shown to be elevated.45–52 For example, ovariectomy or salt loading in SHR increases renal AT1 receptors.44,45 However, renal outer medullary but not cortical AT1 expression has been reported to be increased in SHR relative to WKY.47,48 An autoradiographic study showed increased angiotensin II binding in all areas of the kidney of SHR (relative to WKY) at 1 week of age.49 Renal cortical and brush border membrane AT1 receptor binding is also higher in 4-week-old SHR relative to WKY.50 AT1 receptor expression is higher in certain cerebral nuclei and arteries of adult SHR relative to WKY.51,52 We also find no difference in AT1 receptor protein in RPT cells from WKY and SHR. In contrast, AT1 receptor expression in brush border membranes is higher in SHR than in WKY.53 It is possible that discrepancies in published studies may be related to differences in membrane preparation.
In summary, we have demonstrated that activation (constitutively or via their respective ligands) of D5 and AT1 receptors negatively regulates the expression of each other. Taken together with our previous studies on the negative interaction between D1/D3 receptors on the one hand and AT1 receptors on the other, dopamine receptors and AT1 receptors may counter-regulate each other. Such a counter-regulation may have important implications in the regulation of sodium excretion and blood pressure.
Perspectives
Dopamine, mainly via D1-like receptor (D1 and D5), increases sodium excretion by inhibition of NHE3, Na+-K+ ATPase, Cl–/HCO3–, and Na+/HCO3– exchanger activities. Conversely, angiotensin II, via AT1 receptor, decreases sodium excretion by stimulation of renal tubular ion transport.1–8 Whereas there is reciprocal dopamine and angiotensin modulation in WKY, this effect is altered in SHR. The faulty D1 receptor cannot counter the effects of AT1 receptors in SHR, and the negative modulating action of angiotensin II on AT1 receptors in WKY is actually reversed in SHR. The net result is enhanced antinatriuresis. Although the D5 receptor continues to be a negative regulator of AT1 in SHR, the decreased expression of D5 receptors compared with WKYs may limit its effectiveness. Transregulation at the protein level, by alterations in protein synthesis or degradation,37 is a mechanism by which these receptors regulate each other.
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Acknowledgments |
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These studies were supported in part by National Institutes of Health (NIH) grants HL 23081, DK 39308, HL68686, DK52612, HL 62211, HL-41618, and HL074940 and by the National Natural Science Foundation of China (30470728).
Received October 10, 2004; first decision November 1, 2004; accepted December 23, 2004.
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