| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of 1 Pediatrics, 5 Physiology and Biophysics, and 4 Medicine, Georgetown University Medical Center, Washington, District of Columbia 20007; 2 Zambon Group, 20091 Bresso (MI), Italy; and 3 Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
D1-like (D1, D5) and
D2-like (D2, D3, D4)
dopamine receptors interact in the kidney to produce a natriuresis and
a diuresis. Disruption of D1 or D3 receptors in
mice results in hypertension that is caused, in part, by a decreased
ability to excrete an acute saline load. We studied
D1-like and D2-like receptor interaction in
anesthetized spontaneously hypertensive rats (SHR) by the
intrarenal infusion of Z-1046 (a novel dopamine receptor
agonist with rank order potency of
D3
D4>D2>D5>D1).
Z-1046 increased glomerular filtration rate (GFR), urine flow, and
sodium excretion in normotensive Wistar-Kyoto rats but not in SHRs. The
lack of responsiveness to Z-1046 in SHRs was not an epiphenomenon,
because intrarenal cholecystokinin infusion increased GFR, urine flow,
and sodium excretion to a similar extent in the two rat strains. We
conclude that renal D1-like and D2-like
receptor interaction is impaired in SHRs. The impaired
D1-like and D2-like receptor interaction in
SHRs is not caused by alterations in the coding sequence of the
D3 receptor, the D2-like receptor expressed in
rat renal tubules that has been shown to be involved in sodium
transport. Because the diuretic and natriuretic effects of
D1-like receptors are, in part, caused by an interaction
with D2-like receptors, it is possible that the decreased
Z-1046 action in SHRs is secondary to the renal D1-like
receptor dysfunction in this rat strain.
D1-like receptors; D2-like receptors; natriuresis; diuresis; cholecystokinin; hypertension
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
SEVERAL CANDIDATE GENES have been shown to be important in the pathogenesis of hypertension in human and rodent models of genetic hypertension, but the etiology of essential hypertension remains to be determined (22). In several models of hypertension, an impairment in the ability of the kidney to regulate fluid and electrolyte balance is important in the pathogenesis of the high blood pressure (12). There is ample evidence that under conditions of moderate sodium loading, endogenous renal dopamine, acting via D1-like dopamine receptors with contributions by D2-like dopamine receptors, is important in the regulation of sodium excretion (13, 17, 18, 29, 37). The five dopamine receptors that have been cloned are expressed in the kidney: two belong to the D1-like family (D1 and D5) and three belong to the D2-like family (D2, D3, and D4) (17, 18). Although dopamine or the selective D1-like receptor agonist fenoldopam elicits a decrease in proximal tubular sodium reabsorption in normal humans or in Wistar-Kyoto (WKY) rats, this effect is not seen in the spontaneously hypertensive rat (SHR) and in humans with essential hypertension (1, 7, 10, 26). In mice, disruption of the D1-receptor gene led to the development of hypertension (1).
However, abnormalities in the D1-like receptor alone may not explain salt-sensitive hypertension. Although D2-like receptors exert an antinatriuretic effect when stimulated independently of D1-like receptors, D1-like and D2-like receptors may participate in complex interactions at different levels and through different mechanisms, resulting in a potentially greater inhibition of the sodium pump (4, 5, 14, 17, 18, 33, 34, 36, 39). For instance, in striatal neurons and proximal tubules (but not in medullary thick ascending limbs or cortical collecting ducts), both D1-like and D2-like receptors were required to inhibit Na+-K+-ATPase activity (4, 5, 33). More recently, we reported that D1-like receptors exerted a renal vasodilatory effect while D2-like receptors exerted a renal vasoconstrictor effect (16), in agreement with the studies of Siragy et al. (37). We also found that costimulation of D1-like and D2-like receptors resulted in a diuresis and a natriuresis greater than stimulation of D1-like receptors alone, as predicted by combined ability of these receptors to inhibit Na+-K+-ATPase activity in renal proximal tubules (4, 16, 33).
We previously showed that disruption of the D3-receptor
gene in mice produces renin-dependent hypertension and impairment in
the excretion of an acute saline load (3). In the SHR,
there is also evidence of a defective interaction between
D1- and D2-like receptors (42).
We, therefore, sought to determine whether the ability of
D1-like and D2-like receptors to inhibit
sodium transport in vivo is impaired in the SHR. We compared
the effect of Z-1046 (a novel dopamine receptor agonist with rank order
potency of D3D4>D2>D5>D1)
(16) on glomerular filtration rate (GFR), urine flow (V),
and absolute (UNaV) and fractional (FENa)
sodium excretion between the WKY rat and its hypertensive counterpart,
the SHR. We also studied the coding sequence and expression of the
D3 receptor, the D2-like receptor expressed in
renal tubules involved in sodium transport (17, 23, 27).
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Male WKY and SHRs (12-16 wk old) were maintained on a
regular Purina rat chow diet and unlimited water intake. Food but not water was then withheld 24 h before the study. The rats were
anesthetized with pentobarbital sodium (50 mg/kg body wt), placed on a
heated table to maintain rectal temperature at ~37°C, and
tracheotomized (PE-240) (16). Catheters (PE-50) were
placed into the external jugular and femoral veins and left carotid
artery for fluid administration and blood pressure monitoring. Systemic
blood pressure was monitored electronically using Cardiomax II
(Columbus Instruments, Columbus, OH). Laparotomy was performed to
expose the left and right ureters, which were then catheterized for
urine collection. The right suprarenal artery (which originates from
the right renal artery) was located and catheterized (PE-10, heat
stretched to 180 µm). In some animals, a Transonic Systems flow probe
was secured around the right renal artery (Transonic Systems, Ithaca,
NY); the abdomen was closed with surgical clips. Fluid losses
throughout the experiment were replaced with 5% albumin at 1% body wt
over 30 min. The animals then received an intravenous infusion of
saline containing [14C]inulin (0.01 mCi/10 ml infusate;
New England Nuclear, Boston, MA) at a rate of 5 ml · 100 g body
wt
1 · h1 for 30 min, followed by a
rate of 0.8 ml · 100 g body
wt1 · h1 until the end of the
experiment for determination of GFR. After an equilibration period of
120 min, 40-min urine collections for clearance determinations were
begun, and eight collections were obtained. The rats were killed with
pentobarbital sodium (100 mg/kg) at the end of the experiment. In some
animals, after pentobarbital sodium anesthesia and blood pressure
determination, the kidneys were harvested for immunoblotting and RNA studies.
Renal Function Studies
Control group. The vehicle, normal saline, was infused alone into the right suprarenal artery at a rate of 40 µl/h for eight collection periods for both the hypertensive and normotensive rats. The control group for normotensive rats, concurrently performed with the current studies, was published (16).
Z-1046 group.
On the basis of previous studies that determined the dose of Z-1046
that produced a natriuresis (16), these group of rats received the preferential D3 agonist, Z-1046, at 2 µg · kg1 · min1 for three
periods after two baseline periods where the vehicle, normal saline,
was infused. Subsequently, three more collections were made during the
recovery period, during which the vehicle alone was again infused. The
infusate was changed 10 min before each period to account for the dead
space in the renal arterial catheter. All infusions were given at a
rate of 40 µl/h.
Cholecystokinin group.
To determine whether there is receptor selectivity in any differential
effect of Z-1046 between WKY and SHRs, we also tested the effect of
cholecystokinin. Cholecystokinin receptors, similar to
D1-like receptors, are linked to GS
and
Gq (2, 17). After two baseline periods with
vehicle infusion, cholecystokinin was given to achieve a final renal
arterial blood concentration of 107 mol/l for three
periods. Thereafter, the infusate was changed to the vehicle during the
recovery period as in the Z-1046 group.
Immunoblotting Studies
The antipeptide polyclonal affinity-purified rabbit anti-rat D3 antibody was raised against the specific 19 amino acids in the third cytoplasmic loop of the D3-dopamine receptor at a concentration of 1 µg/µl (D3R12-A, Alpha Diagnostic International, San Antonio, TX). Membranes derived from kidney homogenates or brush-border membranes (BBM) were mixed with Laemmli sample buffer, boiled for 5 min, subjected to electrophoresis on 7.5% SDS-PAGE, and transferred electrophoretically to nitrocellulose membranes. Nonspecific binding was blocked with 10% nonfat dry milk in Tris-HCl-saline-Tween 20 buffer. The membrane was then probed with the D3 primary antibody (1:250) for 1 h. After three washes, the membrane was incubated with peroxidase-labeled anti-rabbit IgG donkey serum (Amersham, Arlington Heights, IL) with 2% normal donkey serum for 60 min. In some studies, the D3 antibodies were preadsorbed with the immunizing peptide #D3R12-P (1 µg/5 µg incubated for 24 h at 4°C). Specific bands were visualized using enhanced chemiluminescence (ECL Western Blotting Detection Kit, Amersham, Arlington Heights, IL). Human embryonic kidney cells transfected with the D3-dopamine receptor cDNA and rat olfactory tubercle were used as positive controls. The specific bands were quantified using Quantiscan (Biosoft, Ferguson, MO) with the total area arbitrarily set at 100% (3).Sequencing Studies
Total RNA was extracted from the kidney of SHR or WKY rats using the RNAzol B (Tel-Test, Friendswood, TX). Total RNA (1 µg) was reverse-transcribed using avian myeloblastosis virus reverse transcriptase (Promega, Madison, WI) at 42°C for 30 min using D3-specific primer 5'-CGAAGTGGGTAAAGGGAGTG-3' (complementary to nt 1800-1819). Subsequently, PCR was performed to amplify the coding region of the rat D3-receptor mRNA [5'-ATGGCACCTCTGAGCCAGATAAGCAC-3' (nt 82-108) and 5'-GCAGGACAGGAT CTTGAGGAAGGC-3' (complementary to nt 1756-1779)]. Another set of primers, 5'-GGAGTCTGGAATTTCAGC-3' (nt 721-738) and 5'-GCCGTGCTGATAGTGAAC-3' (complementary to nt 847-864), was used to confirm the results (GenBank accession number A17753). The PCR products were sequenced using the Applied Biosystem 377 DNA sequencer (Perkin Elmer, Wellesley, MA).Statistical Analyses
The data are expressed as means ± SE. Comparison within groups was made using ANOVA for repeated measures and comparison among groups was made using ANOVA with Newman Keuls test. Measurements between different periods were compared using paired t-test with Bonferroni correction. Corresponding periods between two different groups were analyzed using independent t-test. A P < 0.05 was considered significant.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Effect of Vehicle on Renal Function in the SHR
Intrarenal arterial infusion of the vehicle on the right kidney of the SHRs (n = 5) had no effect on mean arterial pressure (MAP), GFR, V, UNaV, FENa (Table 1), or renal blood flow (not shown). Likewise, the vehicle did not affect renal function in the WKY rats (16).
|
Effect of Z-1046 Infusion on Renal Function
Intrarenal arterial infusion of Z-1046 at a dose of 2 µg · kg1 · min1 did not
affect the MAP or heart rate in either group of animals. However,
Z-1046 increased V, UNaV, FENa, and GFR in WKY
rats (Table 2) but not in SHRs (Tables
3 and 4).
Z-1046 did not alter these variables in SHRs whether basal
sodium excretion was the same as or higher than in the WKY
rats.
|
|
|
Effect of Cholecystokinin Infusion on Renal Function
To determine whether the failure of the kidney of the hypertensive rat to respond to Z-1046 was an epiphenomenon, we studied the effects of the intrarenal arterial infusion of cholecystokinin. Cholecystokinin induced a natriuresis and diuresis (Tables 5-7) in both WKY and SHRs. The natriuretic and diuretic effects of cholecystokinin were evident in SHRs whether basal sodium excretion was the same as or higher than in the WKY rats. Because the baseline V, UNaV, FENa, and GFR were slightly different between WKY and SHRs, we also expressed the effects of cholecystokinin as percent maximum response compared with baseline period 2. The maximum increases in V, UNaV, FENa, and GFR after cholecystokinin were not different among the groups, regardless of whether basal sodium excretions were the same or higher in SHRs compared with WKY rats. (Fig. 1).
|
|
|
|
D3-Receptor Expression and Sequence in WKY and SHRs
To determine whether the decreased response to the preferential D3 agonist Z-1046 observed in the SHR is due to decreased D3-receptor protein expression, we compared D3 protein expression in renal cortical and BBMs between the two groups of rats. Two specific bands were found (
90 kDa and 45 kDa; Fig.
2, A and B); 100
kDa, and 50 kDa have been described in rat brain (21) and 57 kDa in rat kidney (23). The 90-kDa
D3-receptor protein was similar in WKY and SHRs. However,
45-kDa D3-receptor protein was less in SHR than in WKY
(Fig. 2C). The bands were specific because they were
completely or almost completely blocked when the antibodies were
preadsorbed by the immunizing peptide (Fig. 2, A and
B). The sequence of the coding region of the D3
receptor in SHR and WKY rats was identical to the published sequence
(GenBank accession number A17753; data not shown).
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Our studies show that the ability of Z-1046, a dopamine receptor
agonist with the rank order potency D3
D4>D2>D5>D1, to
increase V, UNaV, FENa, and GFR in the
normotensive WKY rat is not present in its hypertensive counterpart the
SHR. Previous studies in our laboratory have shown that the natriuretic
and diuretic effects of Z-1046 are D1- and
D2-like receptor mediated (16). Thus the infusion of the D1-like antagonist SCH-23390 or the
D2-like antagonist domperidone prevented the natriuresis
and diuresis caused by Z-1046 alone in the WKY rat. In the same study,
it was shown that the increase in GFR with Z-1046 was caused by a
D1-like receptor action (16). The inability of
Z-1046 to affect renal function in the SHR is consistent with an
impaired interaction between D1- and D2-like receptors.
Several studies have shown an impaired function of the D1-like receptor in the kidney in rodent genetic and human essential hypertension (6-10, 17, 18, 24, 26). The defective D1-like function in the kidneys of SHRs is caused by an uncoupling of the D1-dopamine receptor from its G protein/effector complex (see review, Refs. 17, 18). The uncoupling has been suggested to be caused by a "hyper" serine phosphorylation of the D1 receptor (31, 43). An important role of the D1-receptor gene in regulating blood pressure was supported by the development of hypertension in mice in which the D1-receptor gene was disrupted (1). It is possible that the failure of the preferential D2-like agonist Z-1046 to alter GFR or produce a diuresis and natriuresis in the SHR was caused by a defective D1 receptor that prevented a normal interaction with the D2-like receptor (4, 16, 19, 23, 33, 34, 42). In the current studies, Z-1046 also had no effect on renal blood flow in the SHR (data not shown).
D2-like receptors have been shown in cells and in
tissues in vitro to increase the inhibition of the sodium pump via
synergistic interactions with D1-like receptors (4,
5, 30, 33). In vivo, in the WKY rat, the D2-like
antagonist domperidone prevented the expected Z-1046-stimulated
natriuresis and diuresis seen, indicating participation of
D2-like receptors (16). The major D2-like receptor expressed in rat renal proximal tubules
and renal vessels is the D3 receptor (17, 23,
27). D2 receptors in the kidney appear to be located
prejunctionally in dopaminergic nerves (11, 17), and the
D4 receptor is mainly expressed in collecting ducts
(17, 40). D3 but not D2 long
receptors have been identified in rat juxtaglomerular cells, and there
is evidence that the D3 receptor may be the dopamine
receptor subtype responsible in regulating renin release
(32). Mice whose D3-receptor gene has been
disrupted exhibit renin-dependent hypertension (3). Increased activity of the renin-angiotensin system resulting in increased reabsorptive action in the kidney has been reported in the
SHR (41). Thus a defective action of D3
receptors in the kidney of the SHR may play a role in the pathogenesis
of the hypertension in this rat strain. The exact defect in the
D3 receptor is not clear from these studies. However, it is
not due to differences in D3-receptor sequence between WKY
and SHRs. Two molecular sizes, 45 and 90 kDa, were observed in
the renal BBM of both WKY and SHRs. There were no differences in the
90-kDa protein between WKY and SHR. However, less 45-kDa
D3-receptor protein was found in the BBM of SHRs. The cause
of the differences in one size but not in another was not determined in
these studies.
The apparent lack of responsiveness of the SHR to Z-1046 infusion is
not an epiphenomenon, because the diuretic and natriuretic effects of
cholecystokinin seen in the WKY rats were also observed in the SHRs.
The effects of parathyroid hormone on cAMP and phosphate excretions
were also similar in WKY and SHRs (28). Cholecystokinin-A receptors and parathyroid hormone receptors, similar to
D1-like receptors, are linked to GS and
Gq/11 (2, 17). Polymorphisms in
GS- and G
-subunits have been reported in some
populations with essential hypertension (15, 35). However,
of these receptors, only D1-like receptor function is
impaired in the kidney in genetic hypertension, suggesting that G
protein dysfunction is probably not a critical component in the rodent
models of genetic hypertension and human essential hypertension
(17, 32).
In conclusion, we showed that the natriuresis and diuresis caused by Z-1046, a dopamine receptor agonist with preferential affinity at D2-like more than D1-like receptors, are abrogated in the SHR. This deficiency was receptor specific, because renal functional effects of cholecystokinin acting at another G protein-coupled receptor, were intact in the SHR.
Perspectives
Abnormal regulation of blood pressure by dopamine receptor subtypes has been reported in genetic hypertension (17, 18). In the SHR, we have reported that the uncoupling of the D1-like receptors, specifically the D1 subtype, in renal proximal tubules from its G protein/effector complex is important in the pathogenesis of hypertension (17, 18, 31). However, abnormalities of D2-like receptors have also been described in genetic hypertension (21, 38). D1- and D2-like receptors may interact to regulate cardiovascular and renal function (4, 5, 16, 33). We now report that there is an impaired interaction in the kidney of D1- and D2-like receptors in the SHR, resulting in impaired renal vasodilatory, diuretic, and natriuretic effects of a dopamine receptor agonist with selectivity to all the dopamine receptor subtypes but not to other G protein-coupled receptors (16). The major renal tubular D2-like receptor is the D3 receptor (reviewed in Refs. 17, 18, 23, 27). The absence of any differences in D3 sequence between WKY and SHRs suggests a primary abnormality of the D1-like receptor. There is also a possibility that the D3 receptor shares a similar posttranslational modification with the D1 receptor that results in impaired renal dopamine receptor function. D3 receptors can form homo-oligomers depending on where the receptors are expressed: the brain striatum expresses oligomers, whereas only monomers are expressed in the ventral midbrain (19, 25). Jung et al. (19) suggested that the D3 autoreceptors may be expressed only as monomers. The significance of the decreased expression of monomeric D3 receptors in the SHR remains to be determined. However, a decreased D3-autoreceptor function may be a mechanism for an increased sympathetic activity in the SHR. D1 receptors have been reported to upregulate D3 receptors but not vice versa (20). Whether the defective D1-receptor function in the SHR has a role in the differential expression of the 45-kDa D3-receptor protein remains to be determined. It is also not known whether the renal D3 receptor shares with the renal D1 receptor the same abnormalities in posttranslational modification (e.g., serine phosphorylation) seen in genetic hypertension (31, 43).| |
ACKNOWLEDGEMENTS |
|---|
These studies were supported in part by Grant HL-58536 from the National Heart, Lung, and Blood Institute and by a National Kidney Foundation Grant, National Capital Affiliate.
| |
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: P. A. Jose, Dept. of Pediatrics, Georgetown Univ. Medical Center, 3800 Reservoir Road NW, Washington, DC 20007 (E-mail: pjose01{at}.georgetown.edu).
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 8 March 2000; accepted in final form 22 May 2001.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Albrecht, FE,
Drago J,
Felder RA,
Printz MP,
Eisner GM,
Robillard JE,
Sibley DR,
Westphal HJ,
and
Jose PA.
Role of the D1A dopamine receptor in the pathogenesis of genetic hypertension.
J Clin Invest
97:
2283-2288,
1996[ISI][Medline].
2.
Alexander SPH and Peters JA. 1999 Receptor and Ion Channel
Nomenclature Supplement. Trends Pharmacol Sci 28:
1999.
3.
Asico, LD,
Ladines C,
Fuchs S,
Accili D,
Carey RM,
Semeraro C,
Pocchiari F,
Felder RA,
Eisner GM,
and
Jose PA.
Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.
J Clin Invest
102:
493-498,
1998[ISI][Medline].
4.
Bertorello, A,
and
Aperia A.
Inhibition of proximal tubule Na+-K+-ATPase activity requires simultaneous activation of DA1 and DA2 receptors.
Am J Physiol Renal Fluid Electrolyte Physiol
259:
F924-F928,
1990
5.
Bertorello, AM,
Hopfield JF,
Aperia A,
and
Greengard P.
Inhibition by dopamine of Na+/K+ ATPase activity in neostriatal neurons through receptor synergism.
Nature
347:
386-388,
1990[Medline].
6.
Chatziantoniou, C,
Ruan X,
and
Arendhorst WJ.
Defective G protein activation of the cAMP pathway in rat kidney during genetic hypertension.
Proc Natl Acad Sci USA
92:
2924-2928,
1995
7.
Chen, CJ,
Vyas SJ,
Eichberg J,
and
Lokhandwala MF.
Diminished phospholipase C activation by dopamine in spontaneously hypertensive rats.
Hypertension
19:
102-108,
1992
8.
Debska-Slizien, A,
Ho P,
Drangova R,
and
Baines AD.
Endogenous dopamine regulates phosphate reabsorption but not Na K-ATPase in spontaneously hypertensive rat kidneys.
J Am Soc Nephrol
5:
1125-1132,
1994[Abstract].
9.
De Vries, PA,
Navis G,
de Jong PE,
de Zeeuw D,
and
Kluppel CA.
Impaired renal vascular response to a D1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats.
J Cardiovasc Pharmacol
34:
191-198,
1999[ISI][Medline].
10.
Felder, RA,
Seikaly MG,
Cody P,
Eisner GM,
and
Jose PA.
Attenuated renal response to dopaminergic drugs in spontaneously hypertensive rats.
Hypertension
15:
560-569,
1990
11.
Gao, D-Q,
Canessa LM,
Mouradian MM,
and
Jose PA.
Expression of the D2 subfamily of dopamine receptor genes in kidney.
Am J Physiol Renal Fluid Electrolyte Physiol
266:
F646-F650,
1994
12.
Guyton, AC,
Coleman TG,
Cowley AW, Jr,
Scheel KW,
Manning RD, Jr,
and
Norman RA, Jr.
Arterial pressure regulation: overriding dominance of the kidneys in long-term regulation and in hypertension.
Am J Med
52:
584-594,
1972[ISI][Medline].
13.
Hegde, SS,
Jadhav AL,
and
Lokhandwala MF.
Role of kidney dopamine in the natriuretic response to volume expansion in rats.
Hypertension
13:
828-834,
1989
14.
Hussain, T,
Abdul-Wahab R,
and
Lokhandwala MF.
Bromocriptine stimulates Na+, K+-ATPase in renal proximal tubules via the cAMP pathway.
Eur J Pharmacol
321:
259-263,
1997[ISI][Medline].
15.
Jia, H,
Hingorani AD,
Sharma P,
Hopper R,
Dickerson C,
Trutwein D,
Lloyd DD,
and
Brown MJ.
Association of the GS gene with essential hypertension and response to -blockade.
Hypertension
34:
8-14,
1999
16.
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
17.
Jose, PA,
Eisner GM,
and
Felder RA.
The renal dopamine receptors in health and hypertension.
Pharmacol Ther
80:
149-182,
1998[ISI][Medline].
18.
Jose, PA,
Eisner GM,
and
Felder RA.
Renal dopamine and sodium homeostasis.
Curr Hypertens Rep
2:
174-183,
2000[Medline].
19.
Jung, MY,
Skryabin BV,
Arai M,
Abbondanzo S,
Fu D,
Brosius J,
Robakis NK,
Polites HG,
Pintar JE,
and
Schmauss C.
Potentiation of the D2 mutant motor phenotype in mice lacking dopamine D2 and D3 receptors.
Neuroscience
91:
911-924,
1999[ISI][Medline].
20.
Levavi-Sivan, B,
Park BH,
Fuchs S,
and
Fishburn CS.
Human D3 dopamine receptor in the medulloblastoma TE671 cell line: cross-talk between D1 and D3 receptors.
FEBS Lett
439:
138-142,
1998[ISI][Medline].
21.
Li XX, Bek M, Asico LD, Yang Z, Grandy DK, Goldstein DS, Rubinstein M,
Eisner GM, and Jose PA. Disruption of the D2 dopamine
receptor produces adrenergic and endothelin B receptor-dependent
hypertension. Hypertension In press.
22.
Lifton, RP.
Molecular genetics of human blood pressure variation.
Science
272:
676-680,
1996[Abstract].
23.
Luippold, G,
Kuster E,
Joos TO,
and
Mühlbauer B.
Dopamine D3 receptor activation modulates renal function in anesthetized rats.
Naunyn Schmiedebergs Arch Pharmacol
358:
690-693,
1998[ISI][Medline].
24.
Masuzawa, K,
Matsuda T,
and
Asano M.
Decreased arterial responsiveness to multiple cyclic AMP-generating receptor agonists in spontaneously hypertensive rats.
Br J Pharmacol
96:
227-235,
1989[ISI][Medline].
25.
Nimchinsky, EA,
Hof PR,
Janssen WGM,
Morrison JH,
and
Schmauss C.
Expression of dopamine D3 receptor dimers and tetramers in brain and in transfected cells.
J Biol Chem
272:
29229-29237,
1997
26.
O'Connell, DP,
Ragsdale NV,
Boyd DG,
Felder RA,
and
Carey RM.
Differential human renal tubular responses to dopamine type 1 receptor stimulation are determined by blood pressure status.
Hypertension
29:
115-122,
1997
27.
O'Connell, DP,
Vaughan CJ,
Aherne AM,
Botkin SJ,
Wang Z-Q,
Felder RA,
and
Carey RM.
Expression of the dopamine D3 receptor protein in the rat kidney.
Hypertension
32:
886-895,
1998
28.
Onsgard-Meyer, MJ,
Berndt TJ,
Khraibi AA,
and
Knox FG.
Phosphaturic effect of parathyroid hormone in the spontaneously hypertensive rat.
Am J Physiol Regulatory Integrative Comp Physiol
267:
R78-R83,
1994
29.
Pelayo, JC,
Fildes RD,
Eisner GM,
and
Jose PA.
Effects of dopamine blockade on renal sodium excretion.
Am J Physiol Renal Fluid Electrolyte Physiol
245:
F247-F253,
1983.
30.
Piomelli, D,
Pilon C,
Giros B,
Sokoloff P,
Martres MP,
and
Schwartz JC.
Dopamine activation of the arachidonic acid cascade as a basis for D1/D2 receptor synergism.
Nature
353:
164-167,
1991[Medline].
31.
Sanada, H,
Jose PA,
Hazen-Martin D,
Yu P-Y,
Xu J,
Bruns JE,
Phipps J,
Carey RM,
and
Felder RM.
Dopamine-1 receptor defect in renal proximal tubular cells in essential hypertension.
Hypertension
33:
1036-1042,
1999
32.
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.
33.
Satoh, T,
Cohen HT,
and
Katz A.
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
34.
Seri, I,
and
Aperia A.
Contribution of dopamine2 receptors to dopamine-induced in-crease in glomerular filtration rate.
Am J Physiol Renal Fluid Electrolyte Physiol
254:
F196-F201,
1988
35.
Siffert, W,
Rosskopf D,
Siffert G,
Busch S,
Moritz A,
Erbel R,
Sharma AM,
Ritz E,
Wichmann HE,
Jakobs KH,
and
Horsthemke B.
Association of a human G-protein 3 subunit variant with hypertension.
Nat Genet
18:
45-48,
1998[ISI][Medline].
36.
Siragy, HM,
Felder RA,
Howell NL,
Chevalier RL,
Peach MJ,
and
Carey RM.
Evidence that dopamine-2 mechanisms control renal function.
Am J Physiol Renal Fluid Electrolyte Physiol
259:
F793-F800,
1990
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
38.
Sowers, JR,
Nyby M,
and
Jasberg K.
Dopaminergic control of prolactin and blood pressure: altered control in essential hypertension.
Hypertension
4:
431-438,
1982
39.
Stier, CT, Jr,
Cowden EA,
and
Allison ME.
Effects of bromocriptine on single nephron and whole kidney function in rats.
J Pharmacol Exp Ther
220:
366-370,
1982
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
41.
Thomas, D,
Harris PJ,
and
Morgan TO.
Age-related changes in angiotensin II-stimulated proximal tubule fluid reabsorption in the spontaneously hypertensive rat.
J Hypertens
6, Suppl4:
S449-S451,
1988.
42.
Vachvanichsanong, P,
Shifra S,
and
Sidhu A.
Absence of DA1/DA2 dopamine receptor interactions in proximal tubules of spontaneously hypertensive rats.
Am J Physiol Renal Fluid Electrolyte Physiol
270:
F98-F105,
1996
43.
Yu, P-Y,
Dirami G,
Hopfer U,
Carey RM,
Felder RA,
and
Jose PA.
Increased serine-phosphorylation of the D1A receptor in renal proximal tubule cells in spontaneous hypertension (Abstract).
Pediatr Res
39:
372A,
1996.
This article has been cited by other articles:
|
|
 |
|
  C. Zeng, I. Armando, Y. Luo, G. M. Eisner, R. A. Felder, and P. A. Jose Dysregulation of dopamine-dependent mechanisms as a determinant of hypertension: studies in dopamine receptor knockout mice Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H551 - H569. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Zeng, Y. Liu, Z. Wang, D. He, L. Huang, P. Yu, S. Zheng, J. E. Jones, L. D. Asico, U. Hopfer, et al. Activation of D3 Dopamine Receptor Decreases Angiotensin II Type 1 Receptor Expression in Rat Renal Proximal Tubule Cells Circ. Res., September 1, 2006; 99(5): 494 - 500. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Zeng, Z. Yang, Z. Wang, J. Jones, X. Wang, J. Altea, A. J. Mangrum, U. Hopfer, D. R. Sibley, G. M. Eisner, et al. Interaction of Angiotensin II Type 1 and D5 Dopamine Receptors in Renal Proximal Tubule Cells Hypertension, April 1, 2005; 45(4): 804 - 810. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Zeng, H. Sanada, H. Watanabe, G. M. Eisner, R. A. Felder, and P. A. Jose Functional genomics of the dopaminergic system in hypertension Physiol Genomics, November 17, 2004; 19(3): 233 - 246. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Zeng, Y. Luo, L. D. Asico, U. Hopfer, G. M. Eisner, R. A. Felder, and P. A. Jose Perturbation of D1 Dopamine and AT1 Receptor Interaction in Spontaneously Hypertensive Rats Hypertension, October 1, 2003; 42(4): 787 - 792. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Felder, H. Sanada, J. Xu, P.-Y. Yu, Z. Wang, H. Watanabe, L. D. Asico, W. Wang, S. Zheng, I. Yamaguchi, et al. G protein-coupled receptor kinase 4 gene variants in human essential hypertension PNAS, March 19, 2002; 99(6): 3872 - 3877. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
