(Hypertension. 1998;32:1049-1053.)
© 1998 American Heart Association, Inc.
Scientific Contributions |
Dopamine D1 Receptor and Protein Kinase C Isoforms in Spontaneously Hypertensive Rats
From the Walter Reed Army Medical Centers (L.P.Y.) and Georgetown University Medical Center, Washington, DC.
Correspondence to Dr Pedro A. Jose, Georgetown University Medical Center 2-PHC, 3800 Reservoir Rd NW, Washington, DC 20007. E-mail josep{at}gunet.georgetown.edu
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Abstract |
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Abstract—Dopamine, via D1-like receptors, stimulates the activity of both protein kinase A (PKA) and protein kinase C (PKC), which results in inhibition of renal sodium transport. Since D1-like receptors differentially regulate sodium transport in normotensive and hypertensive rats, they may also differentially regulate PKC expression in these rat strains. Thus, 2 different D1-like agonists (fenoldopam or SKF 38393) were infused into the renal artery of anesthetized normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (n=5 to 6/drug/strain). Ten or 60 minutes after starting the D1-like agonist infusion, both the infused kidney and the noninfused kidney that served as control were prepared for analysis. The D1-like agonists produced a greater diuresis and natriuresis and inhibited Na+,K+-ATPase activity in proximal tubule (PT) and medullary thick ascending limb (mTAL) to a greater extent in WKY (
20±1%) than in SHR (7±1%, P<0.001).
D1-like agonists had no effect on PKC-
or PKC-
expression in either membrane or cytosol but increased PKC-
expression in PT in both WKY and SHR at 10 minutes but not at 60
minutes. However, membranous PKC-
expression in PT and mTAL
decreased in WKY but increased in SHR with either 10 or 60 minutes of
D1-like agonist infusion. D1-like agonists also
decreased membranous PKC-
expression in PT and mTAL in WKY but
increased it in PT but not in mTAL in SHR. We conclude that there is
differential regulation of PKC isoform expression by
D1-like agonists that inhibits membranous PKC- and
PKC- in WKY but stimulates them in SHR; this effect in SHR is
similar to the stimulatory effect of norepinephrine and
angiotensin II and may be a mechanism for their
differential effects on sodium transport.
Key Words: receptors, dopamine • kidney tubules, proximal • renal medulla • protein kinase C
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Introduction |
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Protein kinase C (PKC) isoforms have been classified into 3 groups: (1) the conventional PKCs (cPKC-
, -ßI, -ßII, and
-
); (2) the novel PKCs (nPKC-, -
, -, -
/G, and -µ); and
(3) the atypical PKCs (aPKC-(
) and -).1
Several of these isoforms have been identified in various nephron
segments.2 3 4 5 6 Thus, proximal tubule (PT)
expresses PKC-, -, -, and -
isoforms,3 and the medullary thick ascending limb
of Henle (mTAL) expresses cPKC- and -ßII, nPKC- and -, and
aPKC- isoforms.4 PKC-, -ß, -, -,
and - were identified in sieved glomeruli, whereas cultured
glomerular epithelial and mesangial cells
express PKC-, -, -, and -.5 PKC-,
-, -, -, and - have been identified in rabbit cortical
collecting duct.6
Dopamine decreases renal sodium transport by adenylyl
cyclase/protein kinase A (PKA) and phospholipase C (PLC)/PKC–dependent
and –independent mechanisms.7 8 9 10 11 12 13 14 However, other
receptors (eg, angiotensin II [Ang II] and -adrenergic
receptors) also increase PKC activity but decrease sodium
excretion.14 15 We have reported that
D1-like receptor agonists increase the expression
and activity of PLC-ß1 but decrease the expression and activity of
PLC- in renal cortical membranes.11
Norepinephrine was also shown to increase expression and
activity of PLC-ß1 but had no effect on PLC- expression or
activity.11 PKC mediates some of the effects of
dopamine, Ang II, and norepinephrine on sodium transport.
Thus, dopamine increases PKC activity and decreases
Na+,K+-ATPase in renal
PT.8 9 12 13 In contrast,
norepinephrine and Ang II increase PKC,
Na+,K+-ATPase,14 15
and Na+/H+ exchanger
activity.15 The mechanism through which these
receptors produce opposing effects in the kidney has not been studied
but may relate to their differing regulation of PKC isoform expression
and activity.
Norepinephrine has been reported to induce the
translocation of PKC-, -ßI, -ßII, -, -, and - but not
PKC- or - from cytosol to membrane in a thyroid cell
line.16 In airway epithelial cells,
1-adrenergic stimulation produced a sustained
translocation of cytosolic PKC- and transient translocation
of PKC- to the membrane.17 Ang II has been
reported to increase the expression of PKC- and - (and possibly
PKC-) in rat PT.3 18 The effect of dopamine
receptor stimulation on PKC isoforms expressed in the kidney has not
been studied. Moreover, a relationship between dopamine
receptor–related PKC isoform expression, sodium excretion, and
Na+,K+-ATPase activity has
not been reported.
The natriuretic effect of dopamine is impaired in genetic hypertension.7 19 This is caused in part by a decreased ability of dopamine via D1-like receptors to stimulate adenylyl cyclase/PKA and PLC/PKC activity.7 The decreased ability of D1-like receptors to stimulate PKC activity in genetic hypertension could be caused by a differential regulation of PKC isoform by dopamine. Therefore, the present study was designed to determine whether D1-like receptors differentially regulate PKC isoform expression in normotensive and hypertensive rats in vivo. The differential effect of D1-like receptors on signal transduction and sodium transport has been noted mainly in PT of these rat strains7,19–21; however, dopamine also decreases sodium pump activity in the mTAL.12 Therefore, studies were performed in the renal cortex, PT, and mTAL. To ensure that any D1-agonist effect is caused by D1-like receptor stimulation, 2 different D1-like receptor agonists (SKF 38393 and fenoldopam) were used. The drugs were infused into the renal artery to obviate any confounding systemic effects.
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Methods |
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Ten- to 16-week-old spontaneously hypertensive (SHR; n=12) and Wistar-Kyoto (WKY; n=13) rats were maintained on standard rat chow until 1 day before the experiment; water was given ad libitum. The rats were anesthetized with pentobarbital (50 mg/kg body wt IP), the temperature was maintained between 36°C and 37°C, and the rats were tracheotomized. Anesthesia was maintained by infusion of pentobarbital at 0.8 mg/100 g body wt per hour. Catheterization of jugular and femoral vessels and left and right ureters and fluid administration were performed as previously described.20 The right suprarenal artery was catheterized, and normal saline was infused at 40 µL/h.20 After a 60-minute equilibration period, a 60-minute urine collection period was begun; then the infusate was changed to SKF 38393 (120 ng · kg-1 · min-1) or fenoldopam (1 µg · kg-1 · min-1) at 40 µL/h.21 The noninfused left kidney served as a concurrent control for the right infused kidney. After 10 or 60 minutes of infusion, the kidneys were removed and the cortex was separated from the medulla. Renal PT and mTAL were obtained by enzymatic digestion, sieving, and differential centrifugation.22 The protein concentrations were determined by the Bradford method.23
Measurement of Na+,K+-ATPase
Activity
Na+,K+-ATPase
activity was measured in PT and mTAL in the noninfused and the SKF
38393–infused kidney by use of tris-p-nitrophenylphosphate
as the substrate.20 This measurement is
relatively insensitive to the endogenous phosphate pool and
to metabolic competition for ATP.
Immunoblot Analysis
Immunoblotting was performed as described
previously.11 The immunoblots
detected by enhanced chemiluminescence (ECL) were quantified by use of
Quantiscan (Biosoft). The percent area of each blot was quantified with
the total area arbitrarily set at 100%.
Data Analysis
Data are expressed as mean±SE. Differences between infused and
noninfused kidney were evaluated by paired t test. When only
2 variables were being compared between groups, differences were
determined by t test. When >2 groups were compared,
differences among groups or within groups were determined by ANOVA or
ANOVA for repeated measures, respectively, and Scheffé's test.
P<0.05 was considered significant.
Materials
Male WKY and SHR (250 to 400 g) were from Taconic Farms
Inc, (Germantown, NY); D1-like agonist fenoldopam
was from Smith Kline Beecham Pharmaceuticals; SKF 38393, Research
Biochemicals International; PKC isozyme antibodies, GibcoBRL and
Upstate Biotechnology Inc; goat anti-mouse or anti-rabbit IgG
conjugated to horseradish peroxidase, Jackson ImmunoResearch Labs, Inc;
and ECL Western blotting detection reagents RPN2106, Amersham Corp. All
other chemicals were from Sigma Chemical Co.
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Results |
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Renal Function Studies
Blood pressure was greater in SHR than in WKY (systolic blood pressure in WKY was 128±1 mm Hg, n=13, and 217±3 mm Hg in SHR, n=10; P<0.05). Urine flow (V) and absolute (UNaV) and fractional sodium excretion (FENa) in the right infused kidney were not different from the left noninfused kidney during the baseline periods (not shown). Sixty-minute infusion of SKF 38393 (SKF) had no effect in the left noninfused kidney but increased V, UNaV, and FENa in the infused right kidney in WKY (V, µL/min: baseline=4.89±0.48, SKF=8.59±0.75; UNaV, nmol/min: baseline=268±64, SKF=589±172; FENa, %: baseline=0.17±0.05, SKF= 0.31± 0.09, ANOVA for repeated measures, baseline versus SKF, right versus left, Scheffé's test) but not in SHR (V, µL/min: baseline=3.73±0.25, SKF=4.46±0.50; UNaV, nmol/min: baseline=377±54, SKF=368±61; FENa, %: baseline=0.24±0.04, SKF=0.22±0.04). The changes in V, UNaV, and FENa due to SKF 38393 in WKY were different from control and were greater in WKY (V=76.32±5.96%, UNaV=113.96±25.94%, FENa=88.05±31.67%) than in SHR (V=21.95±5.50%, P<0.01 versus WKY; UNaV=-1.66±12.74%, P<0.01 versus WKY; FENa=0.73±19.80%, P<0.05 versus WKY). Glomerular filtration rate was not different between WKY and SHR and was not affected by SKF 38393 in either rat strain (data not shown). The effect of the D1-like agonist fenoldopam on V was similar to that obtained with SKF 38393. In WKY, V increased 22% (4.86±0.93 to 6.20±0.98 µL/min, P<0.05, n=5, paired t test) at 10 minutes but was unchanged in SHR (3.36±0.28 to 4.17±0.48 µL/min, P=0.24, n=6, paired t test). At 60 minutes in WKY, V increased 57% (3.17±0.42 to 7.39±0.54 µL/min, P<0.05, n=5, paired t test), whereas in SHR, V increased by only 36% (3.65±0.20 to 5.76±0.24, P<0.05, n=5, paired t test). V at 60 minutes was greater in WKY than in SHR (P<0.05, t test).
Na+,K+-ATPase Activity
SKF 38393 infusion was associated with a greater decrease in
Na+,K+-ATPase activity in
PT and mTAL in WKY than in SHR. Thus, in WKY, SKF 38393 decreased
Na+,K+-ATPase activity in
the right infused kidney by 21.49±0.81% in PT and 18.66±1.27% in
mTAL (compared with the noninfused left kidney, P<0.05,
paired t test). The corresponding values in SHR were
PT=-7.54±0.76% and mTAL=-6.95±0.67%.
Subcellular PKC Isoform Expression in Renal Cortex, PT, and
mTAL
Five PKC isoforms, cPKC- (kDa 80), nPKC- (kDa 80) and -
(kDa 79), and aPKC- (kDa 78) and - (kDa 74) were found in both
cytosolic and membranous fractions of the kidney cortex, PT, and mTAL
from both WKY and SHR. Neither PKC-ß nor PKC- was found in either
WKY or SHR (data not shown).
D1-Like Receptor Agonist Stimulation and PKC
Isoform Expression
Because the decreased ability of dopamine, via
D1-like receptors, to produce a natriuresis in
SHR is in part due to a decreased ability to stimulate PKC
activity,13 19 we measured PKC isoform expression
after infusion of 2 different D1-like agonists,
SKF 38393 and fenoldopam. In the control noninfused kidney, PKC-
expression in membrane but not in cytosol of PT and mTAL was greater in
WKY than in SHR (Figure 1A
and 1B). In PT
and mTAL, SKF 38393 decreased membranous PKC- expression in WKY at
60 minutes; in contrast, in SHR, PKC- increased at 60 minutes
(Figure 1A and 1B). In WKY, another D1-like
agonist, fenoldopam, also decreased PKC- expression in renal
cortical membranes at 10 and 60 minutes: WKY at 10 minutes
(control=27.2±4.0% area, fenoldopam=7.6±0.4% area,
P<0.05, n=4, paired t test) and at 60 minutes
(control=18.0±1.0% area, fenoldopam=6.0±0.6% area,
P<0.05, n=3, paired t test); in contrast, in
SHR, PKC- increased at 10 minutes (control=22.0±1.0% area,
fenoldopam=43.1±4.6% area, n=4, P<0.05, paired
t test) but tended to return to baseline at 60 minutes.
These changes in membranous PKC- expression after fenoldopam
stimulation resulted in reciprocal changes in cytosolic PKC-
expression in both WKY and SHR at 10 minutes (data not shown).
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In the control noninfused kidney, PKC- expression in membrane but
not in cytosol in mTAL but not in PT was greater in WKY than in SHR. In
WKY, 60 minutes of SKF 38393 infusion decreased membranous PKC-
expression in PT and mTAL in a way similar to that noted with PKC-
expression (Figure 2A and 2B). In
contrast, in SHR, membranous PKC- increased in PT but was unchanged
in mTAL. There were no changes in cytosolic PKC- expression in PT or
mTAL in either WKY or SHR. Fenoldopam infusion for 60 minutes also
decreased membranous PKC- expression in renal cortex of WKY
(control=38.1±6.5% area, fenoldopam=10.6±2.3% area, n=3,
P<0.05 paired t test) and tended to increase it
in SHR but did not reach statistical significance (data not shown). In
cytosol, PKC- expression increased in both WKY (control=29.5±5.0%
area, fenoldopam=46.0±6.7% area, P=0.07, n=4, paired
t test) and SHR (control=24.0±5.5% area, fenoldopam
46.6±7.6% area, P<0.05, n=4, paired t test) at
10 minutes. As with SKF 38393, cytosolic PKC- expression was
unchanged at 60 minutes in either rat strain.
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In the control noninfused kidney, PKC-, -, and - expression
was not different between WKY and SHR. The expression of PKC-, -,
or - was not altered by the 60-minute infusion of either
D1-like agonist in renal cortex, PT, or mTAL in
either WKY or SHR (data not shown). However, the 10-minute infusion of
fenoldopam increased membranous PKC- expression in both WKY
(control=18.0±5.1% area, fenoldopam=34.0±4.4% area, n=4,
P<0.05, paired t test) and SHR
(control=17.4±4.7% area, fenoldopam=30.5±4.1% area, n=4,
P<0.05, paired t test).
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Discussion |
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The demonstration of cPKC-
, nPKC- and -, and aPKC- and
- in rat renal cortical and PT subcellular fractions is in agreement
with earlier studies.2 3 4 5 6 In addition, the
present studies demonstrate the presence of nPKC- and - and
aPKC- in mTAL. Our studies also confirm previous reports that failed
to show the expression of cPKC-ß1 and - in rat renal
cortex.2 3 4 5 6
Norepinephrine and Ang II receptor stimulation increase
sodium transport at least in part via increases in PKC
activity.14 15 In normotensive animals, dopamine,
via D1-like receptors, decreases sodium transport
in renal PT in part by the stimulation of PKC
activity.9 12 13 It is not readily apparent how
an increase in PKC activity due to norepinephrine, Ang II,
and dopamine can lead to an increase in sodium transport in one
instance (norepinephrine and Ang II) and a decrease in
another instance (dopamine). The differential effect on sodium
transport may be due to differential effects on PKC isoforms;
D1-like agonists (presumably acting on
D1-like receptors) had no effect on PKC- and
PKC- but decreased PKC- and PKC- expression, the opposite of
the effect of norepinephrine and Ang
II.15 16 17 18 In renal PT, Ang II has been reported
to increase the membranous expression of PKC- and PKC- at high
concentrations and PKC- and PKC- at low
concentrations.3 18
1-Adrenergic stimulation has been reported
also to increase membranous PKC- and PKC-
expression.16 17
The decrease in PKC- and PKC- expression after 60 minutes of
D1-like agonist infusion in WKY is associated
with an increase in sodium excretion and a decrease in
Na+,K+-ATPase activity in
PT in normotensive rats. The role of the decrease in PKC isoform
expression on Na+,K+-ATPase
activity in PT after 60 minutes of D1-like
agonist infusion in normotensive rats remains to be determined since we
did not measure PKC activity. Previous studies have shown that dopamine
and D1-like agonists increase PKC activity in
renal PT,13 14 and they have been suggested as
mediators of inhibition of
Na+,K+-ATPase
activity.12 13 14 However, the dopamine and
D1-like agonist–mediated increase in PKC
activity has been documented only in the first 20 minutes of
stimulation.13 19 Moreover, the effects of PKC
stimulation on
Na+,K+-ATPase activity in
PT vary with time, with an early stimulation followed by an
inhibition.7 Beyond 15 minutes, inhibition of PKC
activity does not affect the ability of dopamine to inhibit
Na+,K+-ATPase activity in
PT.9 These data taken together suggest that
D1-like receptors regulate PKC isoform expression
differently from adrenergic and Ang II receptors. The differential
regulation of PKC isoform expression by these receptors could account
for their differential effect on sodium transport in normotensive
animals. Ang II and 1-adrenergic receptors
increase sodium transport and stimulate
Na+,K+-ATPase activity in
PT, effects opposite of those noted with D1
agonists.14 24 A role of PKC dopamine–mediated
inhibition of Na+,K+-ATPase
activity in mTAL has not been supported by studies that make use of PKC
blockers.12 Our novel finding that
D1-like agonist stimulation is associated with a
decrease in PKC- and PKC- expression in WKY suggests involvement
of PKC in the D1-like action even in this nephron
segment.
There is a defect in the regulation of the
D1-like receptor in the PT in human essential
hypertension and in some models of rodent genetic
hypertension.7 19 20 21 The defect in the
regulation of the D1-like receptor function,
which results in a decreased ability of dopamine to produce a
natriuresis, has been thought to be caused in part by a decreased
ability of dopamine to stimulate PKC activity in renal
PT.19 Recently, PKC isoform gene expression has
been studied in the brain and heart of SHR. These studies showed that
in the cerebral cortex, PKC- mRNA was present in greater
abundance in SHR than in WKY, whereas PKC- mRNA was present in
similar quantities in SHR and WKY. However, in ventricular
myocytes, PKC- mRNA was present in greater abundance in SHR than
in WKY.25 In the renal cortex and PT, we did not
find any differences in PKC isoform expression in the cytosol. However,
membranous PKC- in PT and mTAL and PKC- in mTAL were greater in
WKY than in SHR. The significance of these differences remains to be
determined.
The present studies show that D1-like
receptor stimulation differentially affects PKC isoform expression in
WKY and SHR. Both fenoldopam and SKF 38393 produced a greater
diuresis in WKY than in SHR after 10 and 60 minutes of
infusion. SKF 38393 did not affect renal blood flow or
glomerular filtration rate but increased absolute and
fractional sodium excretion in WKY but not in SHR. As in WKY,
D1-like agonist infusion also did not affect
PKC- and PKC- expression in SHR at 10 or 60 minutes. However,
after 10- or 60-minute infusion of D1-like
agonists, membranous PKC- expression decreased in renal cortex, PT,
and mTAL of WKY but increased in SHR. Membranous PKC- expression was
also decreased by SKF 38393 in PT of WKY at 60 minutes, the opposite of
that found in SHR. However, fenoldopam increased membranous PKC-
expression at 10 minutes in both WKY and SHR.
Several studies have reported that a dopamine or
D1-like receptor–mediated stimulation of PKC
activity is important in the dopamine or D1-like
receptor–mediated inhibition of
Na+,K+-ATPase activity in
renal PT in the short-term period, <20
minutes.9 12 13 Moreover, a failure of dopamine
and D1-like agonists to increase PKC activity has
been reported to be a cause of the failure of these ligands to inhibit
Na+,K+-ATPase activity in
renal PT in SHR.13 We have found that
D1-like agonists inhibit the expression of
PKC- and PKC- in WKY but stimulate it in SHR at 10 and 60
minutes. The only PKC isoform we found to be stimulated by
D1-like agonist is PKC-. It is unlikely that
this PKC isoform is responsible for the short-term stimulation of PKC
activity and inhibition of
Na+,K+-ATPase activity in
renal PT by dopamine and D1-like agonists because
PKC- was increased in both SHR and WKY, yet a diuresis
caused by fenoldopam was noted in the latter but not in the former. It
is possible that other PKC isoforms not measured in this study are
responsible for the PKC activation noted with dopamine and
D1-like agonists. This is entirely speculative
since we did not measure total PKC or isoform activity in the kidney of
these rat strains after D1-like agonist
stimulation. Although we did not determine the effect of specific PKC
isoforms on sodium transport, overexpression of PKC- in NIH 3T3
cells caused an increase in sodium/phosphate
cotransport.26 Thus, the differential effect of
D1-like receptors on PKC isoform expression could
in part explain the decreased ability of D1-like
agonists to inhibit renal sodium handling in SHR. It may be noteworthy
that the effect of D1-like receptor stimulation
on PKC isoform expression in SHR is similar to the effects of
norepinephrine and Ang II stimulation in normotensive
rats.3 16 17 18 Because both Ang II and
norepinephrine increase PT sodium transport and stimulate
Na+,K+-ATPase
activity,14 24 similarities in PKC isoform
expression due to these ligands and D1-like
agonists in SHR may explain in part the decreased ability of
D1-like receptors to induce a natriuresis in
SHR.
In conclusion, D1-like receptors regulate PKC isoform expression differently than adrenergic and Ang II receptors. Moreover, D1-like receptor regulation of rat renal PKC isoform expression differs between normotensive and hypertensive rats. The aberrant effect of D1-like agonists in SHR is similar to the stimulatory effect of norepinephrine and Ang II in normotensive rats and may be a mechanism for the decreased natriuretic effect of D1-like receptors in genetically hypertensive rats.
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Acknowledgments |
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This work was supported in part by grants from the National Institutes of Health DK39308, DK52612, and HL23081. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or Department of Defense.
Received July 6, 1998; first decision July 29, 1998; accepted August 19, 1998.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Hofmann J. The potential for isoenzyme-selective modulation of protein kinase C. FASEB J. 1997;11:649–669.[Abstract]
2. Ostlund E, Mendez CF, Jacobsson G, Fryckstedt J, Meister B, Aperia A. Expression of protein kinase C isoforms in renal tissue. Kidney Int. 1995;47:766–773.[Medline] [Order article via Infotrieve]
3.
Karim Z, Defontaine N, Paillard M, Poggioli J. Protein
kinase C isoforms in rat kidney proximal tubule: acute effect of
angiotensin II. Am J Physiol. 1995;269:C134–C140.
4.
Aristimuno PC, Good DW. PKC isoforms in rat medullary
thick ascending limb: selective activation of the 3-isoform by PGE2.
Am J Physiol. 1997;272:F624–F631.
5. Huwiler A, Schulze-Lohoff E, Fabbro D, Pfeilschifter J. Immunocharacterization of protein kinase C isoenzymes in rat kidney glomeruli, and cultured glomerular epithelial and mesangial cells. Exp Nephrol. 1993;1:19–25.[Medline] [Order article via Infotrieve]
6. Wilborn TW, Schafer JA. Differential expression of PKC isoforms in fresh and cultured rabbit CCD. Am J Physiol. 1996;39:F766–F775.
7. Jose PA, Felder RA. What we can learn from the selective manipulation of dopaminergic receptors about the pathogenesis and treatment of hypertension? Curr Opin Nephrol Hypertens. 1996;5:447–451.[Medline] [Order article via Infotrieve]
8.
Bertorello AM, Aperia A. Inhibition of proximal
Na+-K+-ATPase activity
requires simultaneous activation of
DA1 and DA2 receptors.
Am J Physiol. 1990;259:F924–F928.
9. Pinto-do-O PC, Chibalin AV, Katz AI, Soares-da-Silva P, Bertorello AM. Short-term vs sustained inhibition of proximal tubule Na,K-ATPase activity by dopamine: cellular mechanisms. Clin Exp Hypertens. 1997;19:73–86.
10.
Vyas SJ, Jadhav AL, Eichberg J, Lokhandwala MF.
Dopamine receptor-mediated activation of phospholipase C is associated
with natriuresis during high salt intake. Am J Physiol. 1992;262:F494–F498.
11. Yu PY, Asico LD, Eisner GM, Jose PA. Differential regulation of renal phospholipase C isoforms by catecholamines. J Clin Invest. 1995;95:304–308.
12.
Satoh T, Cohen HT, Katz AI. Different mechanism of
renal Na-K-ATPase regulation by protein kinases in proximal and distal
nephron. Am J Physiol. 1993;265:F399–F405.
13. Kansra V, Chen C, Lokhandwala MF. Dopamine causes stimulation of protein kinase C in rat renal proximal tubules by activating dopamine D1 receptors. Eur J Pharmacol. 1995;289:391–394.[Medline] [Order article via Infotrieve]
14.
Baines AD, Drangova R, Ho P. Role of diacylglycerol in
adrenergic-stimulated 86Rb uptake by renal
proximal tubules. Am J Physiol. 1990;258:F1133–F1138.
15. Houillier P, Chambrey R, Achard JM, Froissart M, Poggioli J, Paillard M. Signaling pathways in the biphasic effect of angiotensin II on apical Na/H antiport activity in proximal tubule. Kidney Int. 1996;50:1496–1505.[Medline] [Order article via Infotrieve]
16. Wang XD, Kiang JG, Atwa MA, Smallridge RC. Evidence for the involvement of protein kinase C isoforms in alpha-1 adrenergic activation of phospholipase A2 in FRTL-5 thyroid cells. J Invest Med. 1996;44:566–574.[Medline] [Order article via Infotrieve]
17.
Liedtke CM, Cole T, Ikebe M. Differential activation of
PKC- and - by 1-adrenergic
stimulation in human airway epithelial cells. Am J
Physiol. 1997;273:C937–C943.
18. Poggioli J, Karim Z, Defontaine N, Lazar G, Bodi I, Paillard M. Protein kinase C (PKC) isozymes present in brush border membrane vesicles (BBMV) isolated from rat kidney proximal tubules (PT) are activated by angiotensin II (AII). J Am Soc Nephrol. 1995;6:743. Abstract.
19. Kansra V, Chen CJ, Lokhandwala MF. Dopamine fails to stimulate protein kinase C activity in renal proximal tubules of spontaneously hypertensive rats. Clin Exp Hypertens. 1995;17:837–845.
20.
Eisner GM, Asico LD, Jose PA. Dopamine and
diltiazem-induced natriuresis in the spontaneously hypertensive rat.
Am J Physiol. 1997;273:R317–R323.
21. Albrecht FE, Drago J, Felder RA, Printz MP, Eisner GM, Robillard JE, Sibley DR, Westphal H, Jose PA. Role of the D1A dopamine receptor in the pathogenesis of genetic hypertension. J Clin Invest. 1996;97:2283–2288.[Medline] [Order article via Infotrieve]
22.
Slobodyansky E, Aoki MG, Gaznabi AKM, Aviles DH, Fildes
RD, Jose PA. Dopamine and protein phosphatase activity in renal
proximal tubules. Am J Physiol. 1995;268:F279–F284.
23. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–254.[Medline] [Order article via Infotrieve]
24. Garvin JL. Angiotensin stimulates bicarbonate transport and Na+/K+ATPase in rat proximal tubules. J Am Soc Nephrol. 1991;1:1146–1152.[Abstract]
25. Gao PI, Zhao GS, Yuan XY, Zhao HF, Chen F, Chen SS. Expression of protein kinase C gene in the brain and heart of spontaneously hypertensive rats. Clin Exp Pharmacol Physiol Suppl. 1995;1:S204–S206.
26.
Lehel C, Olah Z, Mischak H, Mushinski JF,
Anderson WB. Overexpressed protein kinase C-delta and -epsilon subtypes
in NIH 3T3 cells exhibit differential subcellular localization and
differential regulation of sodium-dependent phosphate uptake.
J Biol Chem. 1994;269:4761–4766.
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