Published online before print February 9, 2004, doi: 10.1161/01.HYP.0000118958.27649.6f
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(Hypertension. 2004;43:673.)
© 2004 American Heart Association, Inc.
Scientific Contributions |
Dopamine D1 Receptor Augmentation of D3 Receptor Action in Rat Aortic or Mesenteric Vascular Smooth Muscles
From Department of Pediatrics (C.Z., Z.Y., Z.W., L.D.A., G.M.E., P.A.J.), Physiology and Biophysics (Z.Y., P.A.J.), and Internal Medicine (G.M.E.), Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research (D.W., C.S.W., W.J.W.), Georgetown University Medical Center, Washington, DC; Department of Pathology (R.A.F.), Virginia University for the Health Sciences, Charlottesville; Department of Cardiology (C.Z.), Daping Hospital, Third Military Medical University, Chongqing, People’s Republic of China.
Correspondence to Dr Chunyu Zeng, Department of Pediatrics, PHC-2 Georgetown University Medical Center, 3800 Reservoir Road, NW, Washington, DC 20007. E-mail cyzeng1{at}hotmail.com
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Abstract |
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Dopamine is an important modulator of blood pressure, in part, by regulating vascular resistance. To test the hypothesis that D1 and D3 receptors interact in vascular smooth muscle cells, we studied A10 cells, a rat aortic smooth muscle cell line, and rat mesenteric arteries that express both dopamine receptor subtypes. Fenoldopam, a D1-like receptor agonist, increased both D1 and D3 receptor protein in a time-dependent and a concentration-dependent manner in A10 cells. The effect of fenoldopam was specific because a D1-like receptor antagonist, SCH23390 (10-7 M/24 h), completely blocked the stimulatory effect of fenoldopam (10-7 M/24 h) (D3 receptor: control=21±1 density units [DU]); SCH23390=23±2 DU; fenoldopam=33±2 DU; fenoldopam+SCH23390=23±2 DU; n=10). D1 and D3 receptors physically interacted with each other because fenoldopam (10-7 M/24 h) increased D1/D3 receptor coimmunoprecipitation (35±5 versus 65±5 DU; n=8). A D3 receptor agonist, PD128907, relaxed mesenteric arterial rings independent of the endothelium, effects that were blocked by a D3 receptor antagonist, U99194A. Costimulation of D1 and D3 receptors led to additive vasorelaxation. We conclude that the D1 receptor regulates the D3 receptor by physical interaction and receptor expression. D1 receptor stimulation augments D3 receptor vasorelaxant effects. An interaction of D1 and D3 receptors may be involved in the regulation of blood pressure.
Key Words: receptor • dopamine • arteries • blood pressure
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Introduction |
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Dopamine, a well known neurotransmitter in the central nervous system, has recently been characterized as an important modulator of blood pressure, sodium balance, and renal and adrenal function and is relevant to the pathogenesis and/or maintenance of hypertension.1–4 Dopamine receptors are classified into 2 families: the D1-like receptor subfamily includes the D1 and the D5 receptor, while the D2, D3, and D4 receptors belong to the D2-like subfamily. Whereas the D1-like receptors couple to the stimulatory G protein, G
S, and thus activate adenylyl cyclase, all of the D2-like receptors couple to the inhibitory G protein, Gi/GO, and inhibit adenylyl cyclase and calcium channels and modulate potassium channels.1–4 Both D1 and D3 receptors are expressed in vascular smooth muscle cells, and the activation of the D1 receptor relaxes blood vessels and decreases blood pressure.5,6 However, the effect of D3 receptors on resistance vessels is not clear. A low intravenous dose of R(+)-7-hydroxydipropyl-aminotetralin (7-OH-DPAT), a D2-like agonist with a 50-fold selectivity for the D3 over the D2 receptor, constricts postglomerular arterioles without affecting systemic blood pressure.4 A higher dose, however, decreases blood pressure.4 To test the hypothesis that D1 and D3 receptors interact in vascular smooth muscle cells, we studied the effect of fenoldopam, a D1-like receptor agonist, on D1 and D3 receptor expressions in rat thoracic aorta-derived smooth muscle cell line (A10).7 We also studied the effect of D1 and D3 receptor agonists on the wall tension of rat mesenteric arterial rings.
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Methods |
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Cell Culture and Sample Preparation
Embryonic thoracic aortic smooth muscle cells7,8 (passage 10 to 20) from normotensive Berlin-Druckrey IX (A10; CRL 1476, ATCC) were cultured at 37°C in 95% air/5% CO2 atmosphere in Dulbecco modified eagle medium.
A10 cells (80% confluence) and mesenteric arteries from sodium pentobarbital-anesthetized Wistar-Kyoto (WKY) rats (Taconic, Germantown, NY) were homogenized in ice-cold lysis buffer (5 mL/g tissue) (20 mmol/L Tris-HCl, pH 7.4; 2 mmol/L EDTA, pH 8.0; 2 mmol/L EGTA; 100 mmol/L NaCl; 10 µg/mL leupeptin; 10 µg/mL aprotinin; 2 mmol/L phenylmethylsulfonyl fluoride; 1% NP-40), sonicated, kept on ice for 1 hour, and centrifuged at 16 000g for 30 minutes. All samples were stored at -70°C until use. All experiments were approved by the Georgetown University Animal Use and Care Committee.
Immunoblotting
The antibodies are polyclonal, purified, and antipeptides. The rat D1 receptor immunizing peptide (299-GSEETQPFC-307) (Research Genetics)9–12 and the rat D3 receptor immunizing peptide (r288-QPP SPG QTH GGL KRY YSI C-306) are located on the third extracellular loop of their corresponding receptors.13,14 The specificity of these antibodies has been reported.9–14 A10 cells were treated with vehicle (dH2O), a D1-like receptor agonist (fenoldopam) (Sigma, St. Louis, Mo),3,5,6,9–11,15–17 or a D1-like receptor antagonist (SCH23390) (Sigma, St. Louis, Mo)3,11 at the indicated concentrations and times. The transblots were probed with the D3 (1:250) (Alpha Diagnostic International, San Antonio, Tex) or the D1 receptor antibody (Research Genetics) (1:800). The amount of protein transferred onto the membranes was determined by Ponceau-S staining and immunoblotting for -actin.
Immunoprecipitation
A10 cells were incubated with vehicle (dH2O) or fenoldopam (10-7 M) for 24 hours, as described.9,14 Equal amounts of cell lysates (200 µg protein/mL supernatant) were incubated with affinity-purified anti-D1 receptor antibodies (2 µL/mL) for 1 hour and protein-G agarose at 4°C for 12 hours. The immunoprecipitates were suspended in sample buffer (2X sample buffer: 100% glycerol 2.0 mL; 0.5 mmol/L Tris-HCl 2.5 mL, pH 6.8; 10% SDS 4 mL [final concentration=0.14 mmol/L]; 2 mg/mL bromophenol blue 0.5 mL; 2-mercaptoethanol 0.5 mL, added dH2O until total volume 10 mL), boiled for 10 minutes, and subjected to immunoblotting with the D3 receptor antibody. To determine the specificity of the bands found on the immunoblots, preimmune serum of D1 receptor antibody (negative control) and D3 receptor antibodies (positive control) were used as the immunoprecipitates instead of the D1 receptor antibodies.
Immunohistochemistry
The rat mesenteric artery, cleared of blood with ice-cold oxygenated saline and kept in Histochoice (Amresco, Solon, Ohio) for 1 to 2 days at 4°C, were sectioned (4 µm), embedded in paraffin, and mounted on slides.17 The tissue was deparaffinized and rehydrated by successive incubations in xylene, 100% ethanol, 95% ethanol, 75% ethanol, and phosphate-buffered saline. The tissue was then briefly treated with 0.1% Triton X-100, 10 mmol/L sodium citrate (pH 6.0), and blocked sequentially with 5% goat serum in phosphate-buffered saline overnight at 4°C. The tissue sections were incubated with anti-D3 receptor antibody (1:200) at room temperature for 1.5 hours. After staining with Vector VIP substrate kit, the slides were permanently mounted. The primary antibodies, previously incubated with the immunizing peptides (1:10) at 4°C for 12 hours, were used as controls.
Mesenteric Artery Study
A portion of intestine and mesentery removed from male WKY rats (300 to 350 g, n=12) anesthetized with sodium pentobarbital (50 mg/kg) was kept in ice-cold physiological salt solution (PSS). Four segments of third-generation resistance vessels were dissected under an operating microscope (Olympus, SZ40) and mounted as ring preparations on four 40-µm stainless-steel wires in an isometric Mulvany-Halpern small-vessel myograph (model M610M; J.P. Trading, Science Park, Aarhus, Denmark).18 One wire was attached to a force transducer and the other to a micrometer.18,19 This arrangement enabled the wall tension to be measured at a predetermined internal circumference. Both the dissection and mounting of the vessels were performed in ice-cold (4°C) PSS.
After mounting, the arterial ring was equilibrated in PSS for 1 hour at 37°C at a wall tension of 0.1 mN/mm. Based on preliminary data from >100 vessels, we confirmed that a normalized circumference (L0)=0.9 L100 results in maximal active force development. The vessels were studied at L0 in all subsequent protocols.
After testing the constrictor effects of high-potassium PSS (KPSS, 125 mmol/L) or PSS containing 10-5 M norepinephrine, the vessels were rinsed 3 times with fresh PSS and allowed to recover to baseline for 15 minutes. Maximal contraction of the vessel was then achieved with 10-5 M norepinephrine and KPSS. After reaching a plateau, relaxation was induced with 10-5 M of acetylcholine to test endothelium-dependent relaxation. Ligand-induced relaxation was assessed by cumulative addition of drugs to the rings, which were submaximally (50% to 80%) preconstricted with norepinephrine or KPSS.
To test the action of D1 and/or D3 receptors, cumulative concentrations (10-10 to 10-3 M) of a D1-like receptor agonist, fenoldopam, and/or D3 receptor agonists, PD128907 (Sigma)20,21 and 7-OH-DPAT (Sigma),20,22 were added to the arterial rings preconstricted by norepinephrine or KPSS. The receptor specificities of drug effect were determined by incubating the vessels for 30 minutes with a D1-like antagonist, SCH23390 (10-6 M), or the D3 receptor antagonists, U99194 (10-6 M)23 and (+)-UH232 (Tocris Cookson Inc, Ellisville, Mo) (10-6 M).20,24
To investigate the mechanisms of ligand-mediated vasorelaxation, studies were performed in vessels preincubated for 30 minutes with nifedipine (Sigma)25 or apamin (Sigma) (10-6M; a small conductance calcium-activated K+ channel blocker)26 and charybdotoxin (Sigma) (10-6M; a large conductance calcium-activated K+ channel blocker).26
To determine the endothelium dependence of any D1 or D3 receptor agonist-induced relaxation, vessels with or without endothelium were studied. The endothelium was removed by pulling a hair along the vessels; successful denudement of the endothelium was confirmed by an absence of relaxation by acetylcholine.27
To test any interaction between D1 or D3 receptors, PD128907 (10-10 to 10-3M) studies were performed in vessels preincubated for 30 minutes with fenoldopam (10-6M). To confirm the D3 receptor-mediated vasorelaxation, we used 2 other D3 receptor ligands, 7-OH-DPAT20,22 (agonist), and (+)-UH23220,24 (antagonist).
Statistical Analysis
The data are expressed as mean±SEM. Comparison within groups was made by repeated measures ANOVA (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 factorial ANOVA with Duncan test. Corresponding periods between 2 different groups were analyzed by independent t test. Fenoldopam and PD128907 sensitivity are expressed as pED50, which is the (-log) concentration of the drug required to produce 50% of the maximum response. Relaxation responses to fenoldopam and PD128907 are expressed as a percentage decrease from the maximum contractile response. A value of P<0.05 was considered significant.
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Specificity of Receptor Antibodies
Specific D3 receptor (
45 kDa) bands were found in A10 cells (Figure 1, lane 2), because they were no longer visible when the antibodies were pre-adsorbed by the immunizing peptide. The immunoblotting patterns of the D3 and D1 receptors were similar to those in our previous reports.9,11,13,14,17
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D1 Receptors Increase D3 Receptor Protein Expression in A10 Cells
The D1-like receptor agonist, fenoldopam, increased D3 receptor protein in a concentration-dependent and time-dependent manner. The stimulatory effect at 24 hours was evident at 10-9 M (Figure 2A). The stimulatory effect of fenoldopam (10-7 M) was noted at 16 hours and maintained for at least 24 hours (Figure 2B).
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The specificity of fenoldopam as a D1-like receptor agonist was determined by studying the effect of a D1-like receptor antagonist, SCH23390. Consistent with the data shown in Figure 2A and 2B, fenoldopam (10-7 M/24 h) increased D3 receptor protein (control=21±1 DU, fenoldopam=33±2 DU; n=10; P<0.05). SCH23390 (10-7 M) by itself had no effect on D3 receptor protein (23±2 DU) but reversed the stimulatory effect of fenoldopam on D3 receptor protein expression (fenoldopam+SCH23390=23±2 DU; n=10) (Figure 2C). To determine whether there is mutual receptor interaction, A10 cells were treated with PD128907 (10-10 M to 10-5 M) for 24 hours and immunoreactive D1 receptor protein was measured. Unlike the stimulatory effect of D1 receptors on D3 receptor expression, we did not find any effect of D3 receptors on D1 receptor expression (data not shown).
D1-Like Agonist Increases D1 Receptor Protein Expression in A10 Cells
To investigate the effect of a D1-like receptor agonist on the protein expression of its own receptor, A10 cells were incubated with fenoldopam. Immunoblots showed that fenoldopam also increased D1 receptor protein in a time-dependent (2 to 30 hours) and concentration-dependent (10-11 to 10-6 M) manner. The stimulatory effect (24 hours) was evident at 10-8 M. The stimulatory effect of fenoldopam (10-7 M) was noted at 8 hours and maintained for at least 30 hours (Figure 3 A and B).
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D1 Receptor Physically Interacts With the D3 Receptor in A10 Cells
To determine whether there is a physical interaction between the D3 and the D1 receptor, D1 receptors were first immunoprecipitated with anti-D1 receptor antibodies, and then the immunoprecipitates were probed with anti-D3 receptor antibodies. The 45 kDa band, representing the coimmunoprecipitated D3 and D1 receptors, was increased by a 24-hour treatment with fenoldopam (10-7 M) (control=35±5 DU, fenoldopam=65±5 DU; P<0.01, n=8) (Figure 4).
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D3 Receptor Exists in Rat Mesenteric Artery
We also determined whether the D3 receptor is expressed in rat mesenteric arteries. Consistent with the results in A10 cells, the D3 receptor immunoblots of mesenteric artery homogenates also showed a 45-kDa band (Figure 1, lane 1). Immunohistochemistry showed D3 receptors in the tunica media and intima (Figure 5). Both the immunoblotting and immunohistochemistry results were specific, because the immunoblot (Figure 1, lane 1) and immunostaining (Figure 5) were no longer visible when the antibodies were pre-adsorbed with the D3 receptor immunizing peptide.
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Costimulation of D1 and D3 Receptors Has an Additive Vasorelaxant Effect in the Rat Mesenteric Artery
Effect of Agonists
We next determined the effect of D1 and D3 receptor agonists on the wall tension of rat mesenteric artery rings. The D1 (fenoldopam) and D3 receptor agonists (PD128907 and 7-OH-DPAT) had no vasoconstrictor effect but relaxed arterial rings preconstricted with KPSS in a dose-dependent manner; the vasorelaxant effects were evident at 10-6 M (fenoldopam: Emax [maximum relaxation rate]=83%±11%, pED50=5±0.2, n=12; PD128907: Emax=76%±6%, pED50=5±0.1, n=12; 7-OH-DPAT: Emax=87%±2%, pED50=7±0.2, n=4) (Figure 6A). However, the ability of fenoldopam or PD128907 to relax vessels preconstricted with 10-5M norepinephrine was markedly impaired when compared with vessels preconstricted with KPSS (pED50, fenoldopam: norepinephrine=4±0.2, KPSS=5±0.2, P<0.05; pED50; PD128907: norepinephrine=4±0.2, KPSS=5±0.1, n=12, P<0.01).
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The D1 and D3 receptor agonist vasorelaxant effects were endothelium-independent, because the vasorelaxant effects of fenoldopam and PD128907 were not affected by the presence or absence of the endothelium (10-6 M PD128907: with endothelium=25%±4%; without endothelium=24%±6%; 10-6 M fenoldopam: with endothelium=29%±5%, without endothelium=26%±6%, P>0.05, n=12) (Figure 6B and C).
Effect of Antagonists
The vasorelaxant effects of D1 and D3 receptors were specific, because the D1-like receptor antagonist, SCH23390 (2%±1%), D3 receptor antagonists, U99194A (2%±0.02%) and (+)-UH232 (9%±3%), did not have any effect by themselves but blocked the vasorelaxant effects of their respective agonists: fenoldopam (10-6 M) (fenoldopam=29%±5%, fenoldopam+SCH23390=3%±3%, P<0.01, n=12); PD128907 (10-6 M) (PD128907=24%±6%, PD128907+U99194A=4%±2%, P<0.01, n=12), 7-OH DPAT (7-OH-DPAT=90%±2%, 7-OH-DPAT+U99194A=11%±4%, P<0.01, n=4) (Figure 6B, C, and D).
Effect of combined D1 and D3 receptor stimulation is described herein. PD128907-induced vasorelaxation was increased in vessel preincubated with fenoldopam compared with vehicle (% relaxation at 10-6 M: fenoldopam=40%±5%, vehicle=24%±6%, n=12, P<0.01; pED50: fenoldopam=6±0.1, vehicle=5±0.1, n=12, P<0.05; Figure 6E). These data indicate that D1 and D3 receptor have additive vasorelaxant effects.
Mechanism of D1 and D3 receptor-induced vasorelaxation is described herein. In norepinephrine preconstricted vessels, fenoldopam-induced and PD128907-induced vasorelaxation was increased in vessel preincubated for 30 minutes with nifedipine25 (10-6 M), indicating that the decreased vasorelaxant effects of fenoldopam and PD128907 in norepinephrine-preconstricted vessels may be related to a norepinephrine-induced increase in intracellular calcium (Figure 6F and G). The vasodilatory effect of PD128907 was abrogated by apamin and charybdotoxin, indicating involvement of small-conductance and/or large-conductance calcium-activated potassium channels (Figure 6G).
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The effect of D3 receptors on arterial vascular tone is not well understood. Quinpirole, a D3 receptor agonist with a 35-fold selectivity over the D2 receptor, has no vascular relaxant effect on mesenteric arteries.28 Another D3 receptor agonist, pramipexole, with a 60 selectivity over the D2 receptor,20,21 decreases vascular resistance, although part of the effect could be accounted for by an interaction with the D1 receptor.29 In anesthetized rats, the systemic infusion of 7-OH-DPAT, a D3 receptor agonist with a 50-fold selectivity over the D2 receptor,20,21 decreases renal blood flow by postglomerular constriction, resulting in an increase in glomerular filtration rate.4 In conscious dogs, the intrarenal arterial infusion of quinpirole also decreases renal blood flow, but glomerular filtration rate is decreased as well.30,31 The reason for these apparent discrepancies is not clear. However, the effect of D2-like receptors on vascular tone may vary depending on the resisting tone and the arterial segment being studied3 For example, D1 receptor agonist increases the vascular tone of the rat tail artery.32 In other vessels, including the renal artery, D1 receptors are vasodilatory.5,6 Prejunctional D2-like receptors are vasodilatory whereas postjunctional D2-like receptors can induce vasoconstriction when resting vascular tone is low or vasodilation when resting vascular tone is high.3
Our studies show that in the maximally vasorelaxed mesenteric artery, 2 different D3 receptor agonists, PD128907, with a 120-fold selectivity over the D2 receptor,20,21 and 7-OH-DPAT,20,22 have no effect on vascular contractility. However, when the mesenteric rings are preconstricted, the PD128907, 7-OH-DPAT, and fenoldopam, by themselves, cause vasorelaxation. As compared with vessels preconstricted with norepinephrine, the D1 and D3 vasorelaxation is greater in vessels preconstricted with potassium chloride. The ability of norepinephrine to impair the vasodilatory effects of dopamine has been reported.33 The decreased vasodilator effect of D1 agonists in vessels preconstricted with norepinephrine may be caused by an increase of intracellular calcium by activation of 1-adrenergic receptors.34,35 Our studies show that the vasorelaxant effects of fenoldopam (D1 receptor agonist) and PD128907 (D3 receptor agonist) are enhanced by calcium channel blockade with nifedipine. The vasodilatory effect of D3 receptors may also involve potassium channels (small-conductance and/or large-conductance calcium activated potassium).36,37 Additionally, norepinephrine can also compete with the agonists for dopamine receptor occupancy.38,39
The vasorelaxant effect of dopamine in the rabbit pulmonary artery has been reported to be endothelium-dependent and endothelium-independent.40 However, in our studies, despite the presence of D3 receptors in the intima, the vasodilatory effects of the D1 and D3 receptor agonists are endothelium independent. The function of the D3 receptor in endothelial cells is not clear, but D3 receptors have cell-protective properties.41 In human brain endothelial cells,42 the D3 agonist, PD128907, inhibits superoxide production, determined by cytochrome C reduction test,43 an effect that is blocked by a D3 antagonist, U99194A, which by itself does not have any effect (Z. Yang, C. Zeng, K.S. Kim, P.A. Jose, unpublished data, 2003).
The simultaneous stimulation of D1 and D3 receptors causes a vasorelaxation that is additive rather than synergistic. This may indicate that D1 and D3 receptors induce vasorelaxation by different mechanisms. Our studies also indicate that the vasorelaxation of the mesenteric artery is probably caused by activation of postjunctional rather than prejunctional dopamine receptors, because neither D1 receptor nor D3 receptor is expressed in the tunica adventitia, where the nerve supply terminates. The reason for the inability of others to demonstrate D3 receptors in vascular smooth muscles is not clear.44
We find that D1 and D3 receptors coimmunoprecipitate, and that coimmunoprecipitation is increased by D1 receptor stimulation. There are 2 possible explanations for this observation: increased D1 and D3 receptor expression, per se, or an increased physical interaction between D1 and D3 receptors. This interaction occurs only after several hours of treatment and may explain the absence of synergism in the acute studies in mesenteric vessels. Further studies are needed to determine whether the increased interaction between these 2 receptors is a direct or an indirect mechanism. However, homo-oligomerization or hetero-oligomerization of several G protein-coupled receptors have been reported.45,46
In summary, we have demonstrated that the D1 receptor regulates the D3 receptor by physical interaction and receptor expression. D1 receptor stimulation augments D3 receptor vasodilatory effects. A D1/D3 receptor interaction may be involved in the regulation of blood pressure.
Perspectives
The vasodilator effect of dopamine via D1-like receptors is mediated mainly by cAMP/protein kinase A.47,48 It seems paradoxical that the D3 receptor dilates the mesenteric artery because D2-like receptors decrease while D1-like receptors increase cAMP production.1–3 D3 receptors linkage to adenylyl cyclase inhibition is weak, unless adenylyl cyclase V is present.49 Adenylyl cyclase isoform V has been shown in rat pulmonary arterial smooth muscles but not in aortic smooth muscles.50 Therefore, it is likely that the D3 receptor-mediated vasorelaxation in vascular smooth muscle cells is caused by its ability to stimulate K+ channels.36 Under these conditions, the vasorelaxant effects of D1-like receptors caused by cAMP/PKA may be additive to the vasorelaxant effect of D3 receptors caused by stimulation of K+ channels.36,37
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Acknowledgments |
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These studies were supported in part by grants from the National Institutes of Health, HL 074940, HL 23081, DK 39308, HL68686, DK52612, and HL62211.
Received July 16, 2003; first decision August 21, 2003; accepted November 20, 2003.
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References |
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1. Jose PA, Eisner GM, Felder, RA. Dopamine receptor-coupling defect in hypertension. Curr Hypertens Rep. 2002; 4: 237–244.[Medline] [Order article via Infotrieve]
2. Hussain T, Lokhandwala MF. Renal dopamine receptor function in hypertension. Hypertension. 1998; 32: 187–197.
3. Jose PA, Eisner GM, Felder RA. Renal dopamine receptors in health and hypertension. Pharmacol Ther. 1998; 80: 149–182.[CrossRef][Medline] [Order article via Infotrieve]
4. Muhlbauer B, Kuster E, Luippold G. Dopamine D3 receptors in the rat kidney: role in physiology and pathophysiology. Acta Physiol Scand. 2000; 168: 219–223.[CrossRef][Medline] [Order article via Infotrieve]
5. Ventura HO, Messerli FH, Frohlich ED, Kobrin I, Oigman W, Dunn FG, Carey RM. Immediate hemodynamic effects of a dopamine-receptor agonist (fenoldopam) in patients with essential hypertension. Circulation. 1984; 69: 1142–1145.
6. Murphy MB, Murray C, Shorten GD. Fenoldopam: a selective peripheral dopamine-receptor agonist for the treatment of severe hypertension. N Engl J Med. 2001; 345: 1548–1557.
7. Iso T, Chung G, Hamamori Y, Kedes L. HERP1 is a cell type-specific primary target of Notch. J Biol Chem. 2002; 277: 6598–6607.
8. Kimes BW, Brandt BL. Characterization of two putative smooth muscle cell lines from rat thoracic aorta. Exp Cell Res. 1976; 98: 349–366.[CrossRef][Medline] [Order article via Infotrieve]
9. Xu J, Li XX, Albrecht FE, Hopfer U, Carey RM, Jose PA. Dopamine 1 receptor, Gs, and Na+-H+ exchanger interactions in the kidney in hypertension. Hypertension. 2000; 36: 395–399.
10. O’Connell DP, Botkin SJ, Ramos SI, Sibley DR, Ariano MA, Felder RA, Carey RM. Localization of dopamine D1A receptor protein in rat kidneys. Am J Physiol. 1995; 268: F1185–F1197.[Medline] [Order article via Infotrieve]
11. Yu PY, Eisner GM, Yamaguchi I, Mouradian MM, Felder RA, Jose PA. Dopamine D1A receptor regulation of phospholipase C isoform. J Biol Chem. 1996; 271: 19503–19508.
12. Missale C, Nash SR, Robinson SW, Jaber M, Caron MG. Dopamine receptors: from structure to function. Physiol Rev. 1998; 78: 189–225.
13. Ladines CA, Zeng C, Asico LD, Sun X, Pocchiari F, Semeraro C, Pisegna J, Wank S, Yamaguchi I, Eisner GM, Jose PA. Impaired renal D1-like and D2-like dopamine receptor interaction in the spontaneously hypertensive rat. Am J Physiol Regul Integr Comp Physiol. 2001; 28: R1071–R1078.
14. Zeng C, Asico LD, Wang X, Hopfer U, Eisner GM, Felder RA, Jose PA. Angiotensin II regulation of AT1 and D3 dopamine receptors in renal proximal tubule cells of SHR. Hypertension. 2003; 41: 724–729.
15. Murphy MB. Dopamine: a role in the pathogenesis and treatment of hypertension. J Hum Hypertens. 2000; 14: S47–S50.[CrossRef][Medline] [Order article via Infotrieve]
16. Watanabe H, Xu J, Bengra C, Jose PA, Felder RA. Desensitization of human renal D1 dopamine receptors by G protein-coupled receptor kinase 4. Kidney Int. 2002; 62: 790–798.[CrossRef][Medline] [Order article via Infotrieve]
17. Zheng S, Yu P, Zeng C, Wang Z, Yang Z, Felder RA, Jose PA. Differential G protein subunit linkage and regulation of D1 and D5 dopamine receptors in renal proximal tubule. Hypertension. 2003; 41: 604–610.
18. Mulvany MJ, Halpern W. Contractile properties of small arterial resistance vessels in spontaneously hypertensive and normotensive rats. Circ Res. 1977; 41: 19–26.
19. Schiffrin EL, Deng LY, Larochelle P. Blunted effects of endothelin upon small subcutaneous resistance arteries of mild essential hypertensive patients. J Hypertens. 1992; 10: 437–444.[CrossRef][Medline] [Order article via Infotrieve]
20. Levant B. The D3 dopamine receptor: Neurobiology and potential clinical relevance. Pharmacol Rev. 1997; 49: 231–252.
21. Joyce JN. Dopamine D3 receptor as a therapeutic target for antipsychotic and antiparkinsonian drugs. Pharmacol Ther. 2001; 90: 231–259.[CrossRef][Medline] [Order article via Infotrieve]
22. Luippold G, Zimmermann C, Mai M, Kloor D, Starck D, Gross G, Muhlbauer B. Dopamine D(3) receptors and salt-dependent hypertension. J Am Soc Nephrol. 2001; 12: 2272–2279.
23. Kling-Petersen T, Ljung E, Svensson K. Effects on locomotor activity after local application of D3 preferring compounds in discrete areas of the rat brain. J Neural Transm. 1995; 102: 209–220.[CrossRef][Medline] [Order article via Infotrieve]
24. Chu E, Chu TC, Potter DE. Mechanisms and sites of ocular action of 7-hydroxy-2-dipropylaminotetralin: a dopamine3 receptor agonist. J Pharmacol Exp Ther. 2000; 293: 710–716.
25. McHarg AD, Southerton JS, Weston AH. A comparison of the actions of cromakalim and nifedipine on rabbit isolated mesenteric artery. Eur J Pharmacol. 1990; 185: 137–146.[Medline] [Order article via Infotrieve]
26. Kim JH, Shin SY, Yun SS, Kim TJ, Oh SJ, Kim KM, Chung YS, Hong EK, Uhm DY, Kim SJ. Voltage-dependent ion channel currents in putative neuroendocrine cells dissociated from the ventral prostate of rat. Pflugers Arch. 2003; 446: 88–99.[Medline] [Order article via Infotrieve]
27. Schafer A, Burkhardt M, Vollkommer T, Bauersachs J, Munzel T, Walter U, Smolenski A. Endothelium-dependent and -independent relaxation and VASP serines 157/239 phosphorylation by cyclic nucleotide-elevating vasodilators in rat aorta. Biochem Pharmacol. 2003; 65: 397–405.[CrossRef][Medline] [Order article via Infotrieve]
28. Lei S, Orensanz LM, Mulvany MJ, Simonsen U. Mechanisms involved in the vasorelaxant effect of (-)-stepholidine in rat mesenteric small arteries. Eur J Pharmacol. 1999; 365: 193–204.[Medline] [Order article via Infotrieve]
29. Kaneko S, Eisner GM, Jose PA. Effect of pramipexole, a dopamine-1/dopamine-2 receptor agonist, on sodium excretion and blood pressure in spontaneously hypertensive rats. J Auton Pharmacol. 1990; 101: S53–S60.
30. Siragy HM, Felder RA, Peach MJ, Carey RM. Intrarenal DA2 dopamine receptor stimulation in the conscious dog. Am J Physiol. 1992; 262: F932–F938.[Medline] [Order article via Infotrieve]
31. Siragy HM, Felder RA, Howell NL, Chevalier RL, Peach MJ, Carey RM. Evidence that dopamine-2 mechanisms control renal function. Am J Physiol. 1990; 259: F793–F800.[Medline] [Order article via Infotrieve]
32. Rashed SM, Songu-Mize E. Regulation of Na+-pump activity by dopamine in rat tail arteries. Eur J Pharmacol. 1995; 284: 289–297.[CrossRef][Medline] [Order article via Infotrieve]
33. Anwar N, Mason DF. Actions of dopamine and apomorphine on the vasoconstrictor responses of perfused mesenteric arteries of mouse, rat and rabbit. J Pharm Pharmacol. 1981; 33: 150–154.[Medline] [Order article via Infotrieve]
34. Gisbert R, Perez-Vizcaino F, Cogolludo AL, Noguera MA, Ivorra MD, Tamargo J, D’Ocon P. Cytosolic Ca2+ and phosphoinositide hydrolysis linked to constitutively active alpha 1D-adrenoceptors in vascular smooth muscle. J Pharmacol Exp Ther. 2003; 305: 1006–1014.
35. Wilson C, Cooper SM, Buckingham RE, Clapham JC. Alpha 1-adrenoceptor-mediated contraction of rabbit mesenteric artery: a role for intra- and extracellular calcium pools. J Cardiovasc Pharmacol. 1987; 9: 401–406.[Medline] [Order article via Infotrieve]
36. Kuzhikandathil EV, Oxford GS. Dominant-negative mutants identify a role for GIRK channels in D3 dopamine receptor-mediated regulation of spontaneous secretory activity. J Gen Physiol. 2000; 115: 697–706.
37. Werner P, Hussy N, Buell G, Jones KA, North RA. D2, D3, and D4 dopamine receptors couple to G protein-regulated potassium channels in Xenopus oocytes. Mol Pharmacol. 1996; 49: 656–661.[Abstract]
38. Seeman P. Receptor Tables. Drug dissociation constraints for neuroreceptors and transporter. Toronto, Canada: SZ Research; 1993.
39. Seeman P, Schaus JM. Dopamine receptors labelled by [3H]quinpirole. Eur J Pharmacol. 1991; 203: 105–109.[CrossRef][Medline] [Order article via Infotrieve]
40. Yamauchi M, Kobayashi Y, Shimoura K, Hattori K, Nakase A. Endothelium-dependent and -independent relaxation by dopamine in the rabbit pulmonary artery. Clin Exp Pharmacol Physiol. 1992; 19: 401–410.[Medline] [Order article via Infotrieve]
41. Ling ZD, Robie HC, Tong CW, Carvey PM. Both the antioxidant and D3 agonist actions of pramipexole mediate its neuroprotective actions in mesencephalic cultures. J Pharmacol Exp Ther. 1999; 289: 202–210.
42. Chung JW, Hong SJ, Kim KJ, Goti D, Stins MF, Shin S, Dawson VL, Dawson TM, Kim KS. 37-kDa laminin receptor precursor modulates cytotoxic necrotizing factor 1-mediated RhoA activation and bacterial uptake. J Biol Chem. 2003; 278: 16857–16862.
43. Fantuzzi A, Sadeghi S, Valetti F, Rossi GL, Gilardi G. Tuning the reduction potential of engineered cytochrome c-553. Biochemistry. 2002; 41: 8718–8724.[Medline] [Order article via Infotrieve]
44. Amenta F. Light microscope autoradiography of peripheral dopamine receptor subtypes. Clin Exp Hypertens. 1997; 19: 27–41.[CrossRef][Medline] [Order article via Infotrieve]
45. AbdAlla S, Lother H, Quitterer U. AT1-receptor heterodimers show enhanced G-protein activation and altered receptor sequestration. Nature. 2000; 407: 94–98.[CrossRef][Medline] [Order article via Infotrieve]
46. Nimchinsky EA, Hof PR, Janssen WG, Morrison JH, Schmauss C. Expression of dopamine D3 receptor dimers and tetramers in brain and in transfected cells. J Biol Chem. 1997; 272: 29229–29237.
47. Chatziantoniou C, Ruan X, Arendshorst WJ. Defective G protein activation of the cAMP pathway in rat kidney during genetic hypertension. Proc Natl Acad Sci U S A. 1995; 92: 2924–2928.
48. Heesen BJ, DeMey JG. Effects of cyclic AMP-affecting agents on contractile reactivity of isolated mesenteric and renal resistance arteries of the rat. Br J Pharmacol. 1990; 101: 859–864.[Medline] [Order article via Infotrieve]
49. Robinson SW, Caron MG. Selective inhibition of adenylyl cyclase type V by the dopamine D3 receptor. Mol Pharmacol. 1997; 52: 508–514.
50. Jourdan KB, Mason NA, Long L, Philips PG, Wilkins MR, Morrell NW. Characterization of adenylyl cyclase isoforms in rat peripheral pulmonary arteries. Am J Physiol Lung Cell Mol Physiol. 2001; 280: L1359–L1369.
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