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and h as d iffe re nt h emodynam ic con sequ en ce s d ep en din g
o n th e mod el. In th e tw o-k id ne y, o ne -c lamp (2K1C) RVH
model , p la sma-r en in act iv it y i nc reas es , but t he one -k idney
one-clam p (1K 1C ) m odel does not increase piasm a-renin
activity (3). Sodium depletion caused by diuretics may
contribute to the reduction of GFR in the presence of
r enal a rt er y s teno si s (RAS) ( 4) .
Chlorothiazide and hydrochlorothiazide act prim arily
at the cortical diluting site and they can cause the loss of
5 —8 offiltered sodium 5) by increasing urine volum e
and s od ium exc re tio n. T he ir a cti on is q uite d iffe re nt from
fu ro semid e, w hic h a cts a t th e lo op o f H en le . T he re fo re , it
is re aso na ble to e xp ec t th at th e e ffe ct o f d iu re tic th era py
o n th e re su lts o fACE may d ep en d on t he s pe cific d iu re tic
used.
N orm al anim als develop acute sodium diuresis during
the first day of diuretic treatm ent and return to norm al
after lo ng-term treatm en t (6). T he d iuretic effect on the
kidney with RAS is not w ell characterized. A few studies
sug gest th at acu te ad min istratio n of fu ro sem id e in creases
g lome ru la r filtra tio n ra te (G FR ), e ffe ctiv e re na l p la sm a
flow (ER PF) and urinary sodium excretion rate both in
kidneys with and without RAS in rats and in patients (7-
8). Sodium excretion and plasm a volum e depletion follow
ing diuretic treatment in RVH may influence the renin
an gio ten sin sy ste m an d m ay affect th e d iag nostic sensitiv
ity o fA CE I-ind uced ren al insu fficien cy test (9 ,1 0).
The e le va te d ang io te ns in II le ve l in th e c lamped k id ney
c on trib ute s to th e a lte ra tio n o f re na l h emod yn am ic s a nd
tubu lar function (8), w hile the renal hem ody nam ics re
ma in re la tiv ely u nchang ed in th e con tra la te ra l k id ney. In
1K 1C R VH , the renin level increases for a w eek and th en
gradually decreases to normal, but the blood pressure
rem ain s hig h (1 1).
In d iu re tic -tre ate d u nila te ra l RV H, th e d iu re tic a lo ne
may a ffe ct re na l fu nc tio n and re du ce th e s en siti vity o f th e
c ap to pril-in du ce d re na l in su ffic ie nc y te st. A lte rn ativ ely ,
d ep le te d p la sma volume c au sed b y d iu re tic tre atment may
sens it ize the captopr il -induced renal insuff ic iency tes t.
This study was designed to observe the acute and
chro ni c e ffe ct o f d iu re tic tre atment o n c ap to pril-in du ced
functio nal changes in 2K 1C and 1K 1C rats in an effort to
d efin e th e in fl ue nc e o f d iu re tic th er ap y o n th e in te rp re ta
tio n o f a c ap to pril c ha lle ng e in th e d iffe re ntia l d ia gn osis
of R VH .
An ti hype rt en si ve agen ts may mod if y th e r enal e ff ec ts o f an
g io te ns in c on ve rtin g e nz ym e in hib itio n A CE I . T his p ote ntia l
in teract ion, which is important in the diagnosisof renovascular
hype rtension was s tud ied in two r at mode ls w ith and w ithout
diureticreatmentpriorto ACE I.Acuteintravenousdminis
tr at ion o f f ur osem ide o r hydroch lo ro th ia zi de i n one- kidney ,
one-c lamp an ima ls 1K i C d id no t change g lomeru la r f il tr at ion
rate GFR or effectiverenalplasmaflow ERP F .ACE Iad
ministrationfter furosemideand hydrochlorothiazidee
c re as ed G FR p < 0 .0 01 , p < 0 .0 1 b u t n ot ERPF . Ch lo ro th ia
z id e adm in is te re d to 1Ki C p rio r to ACEI, d ec re as ed G FR p
< 0.02) but not ERPF captopril administration to 1 Ki C which
received hydrochloroth iaz ide intraperi toneal ly for 7—1days
d ec re as ed G FR p < 0 .0 07 a nd E RP F p < 0 .0 2 , w hile tw o
k idney, one-c lamp an ima ls 2K1C decreased GFR on ly in the
c lam ped k id ne y p < 0 .0 05 . ERPF in 2K1C in cre as ed only in
t he cont ra la te ra lk idney p < 0 .01 . W i thout d iu re tic I K i C
a nim als d ecre as ed G FR a nd E RP F a fte r A CE I p < 0 .0 05 , P
< 0.001). In the damped kidney of 2K1 C rats, GFR and ERPF
dec re as ed s ig nific an tly p < 0 .0 005, p < 0 .0 04 a nd c on tra
la te ra l k id ne y ERPF in cre as ed p < 0 .0 01 , b ut G FR d id not.
The consequenceso fACEI on GFR are s im il arw i th o r w ithout
diuret ic .These data suggest that diuret ic therapy may not
s ign ific antl y i nte rf er e w ith ACEI eva lua ti on o f r enovascu la r
hypertension
J NucIMed 1992;33:739—743
h e in cre as in g u tiliz atio n o f c ap to pril re no gra ph y h as
raised concerns about possible factors w hich m ay alter the
re su lts o f th is te st. A n tih yp erte ns iv e agents may a ffe ct th e
ren al fu nc tio n ch an ges in du ced b y ang io ten sin co nve rtin g
enzyme in hib it io n (ACE ) in th e d iffe re ntia l d ia gn os is o f
re no va scula r h yp erte ns io n (RVH). A lth ou gh it is w ell e s
tablished that the combined use of a diuretic agent and
cap topr il may induce r ena l i nsuf fi ci ency (1 ,2 ), t he add it iv e
effects of captopril on diuretic agents in RVH have not
been studied extensively. Experimental RVH due to the
con stric tio n o f th e re na l a rte ry is a ng io te ns in -d ep en dent
Rec ei ve d O ct. 1 8, 1 99 1 ; r ev is io n a cc ep te d D ec . 3 0, 1 99 1.
Fo r repr in tscon tac t: M . DonaldB lau fox , MD, PhD,A iber t E ins te in Co ll ege
o f Med ic ine ,1300Mor r is Pa rk Ave ., B rOnX ,NY 10461 .
Captopn lD unng Diure ticTherapy •ee and Blaufox
739
Renal Functional Response to Captopril During
iuretic herapy
Hyo Bok Lee and M . Donald Blaufox
Dep artm en t o fN uc le ar M ed ic in e, A lb er t E in ste in C olle ge o fM ed ic in e/Mo nte fio re M ed ic al C en te r, B ro nx , N ew York
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ERPF weremeasuredwhen urine f lowwas s tab le .Technetium
99m-DTPA(50 @iCi)nd [‘311]orthoiodohippurate(OIH)(30Ci)
m ixed in 10 m l of saline w ere infused w ith a SAGE constant
in fu sio n pu mp at th e sam e flo w rate as the salin e. O nce ste ady
s ta te b lood l eve ls o f 99mTc@DTPAnd [†˜311]OIHere r eached ,
urin e w as co lle cted u sin g 10 -m m co lle ctio n p eriod s fo r each
c lear ance .B lood f rom the f emo ra l a rt er y was ob ta in ed a t t he
midpo in t o feach c lea rance pe ri od usi ng two hepa ri ni zed cap il la ry
tubes. Plasm a sam ples of 0.05 m l and 0. 1 m l urine sam ples
diluted to 3 m l w ith w ater w ere counted in a w ell counter w ith
c ro ss -ta lk c orre ctio n fo r 9 9mT ca nd â €˜M I.h e samp le s w ere re
c ounte d f or â €˜@†˜Ifte r 9 9mT ch ad b ee n a llowe d to d ec ay to b ac k
g round. C le ar an ce v al ue s wer e c alc ula te d by th e s ta nd ar d UV /P
rel at ionsh ip . The b lood pre ssur e was measu red for each c lear ance
pe ri od be fo re t he b lood sample co ll ec ti on .
The m ean values of all three G FR and ERPF values for the
co ntrol an d ex perim en tal p eriod s w ere u sed fo r the ana ly sis.
S ta tis tic al a na ly sis wa s p er fo rmed by S tudent's p ai re d t- te st fo r
each group, and two p values less than or equal to 0.05 w ere
c on sid er ed to b e s ignif ic an t. R eg re ss io ns we re c alc ul ate d u sing
one -way ana ly si s o f v ar ia nc e. S igni fi ca nc e o f c or re la tio ns was
de te rmined f rom Pear son 's r ank orde r coef fi ci en ts .
RE SUL T S
A c u te Diu re tic E ffe c ts o n G FR a n d E RP F
A cute in travenous injection of furosem ide or H CT Z
alone in the 1K1C model did not significantly change
G FR or E RP F. T he contro l and post-furosem id e trea ted
GFRs were 0.34 ml/min/100 g BWT ±0.03 (s.e.) and
0.30 ±0.02 (ns), respectively. The GFR of control and
HCTZ -tre ate d anima ls w ere 0 .3 8 ±0 .0 5 and 0 .3 8 ±0 .0 5
(n s), re sp ec tiv ely . T he c on tro l a nd fu ro semid e-tre ate d
ER PF s w ere 1.25 Â ±0. 10 and 1.06 Â ±0.06 (ns), and the
HCTZ-treated group ERPFs were 1. 17 ±0. 13 and 1. 15 ±
0 . 13 n s ), r e s p e c t iv e l y . ig n if ic a n tc h a n g e sin re n a l f u n c
tio n w ere o bse rv ed in b oth g ro up s a fte r a cu te a dm in istra
t ion o fcap topr il f ol low ing f ur os emide o r HCTZ t reatmen t.
The G FR of the furosem ide-treated group fell to 0.23 Â ±
0 .0 2 , p < 0 .0 0 1 ) a nd th a t o f th e HC TZ -t re ate d g ro u p fe ll
to 0 .2 7 ±0 .0 4 ( p < 0 .0 1). I n th e g ro up o fa nima ls re ce iv in g
CTZ in drinking water overnight, the GFR fell from 0.39
±0.02 to 0.25 ±0.06 (p < 0.02) after captopril treatm ent.
ACE a fte r d iu re tic t re atment d id n ot s ig nific an tly a ffe ct
E RPF in any of the thr ee gr oups Fig. 1).
1K 1C anim als that did not receive diuretics prior to
captopnl had a control GFR and ERPF of 0.36 ±0.02
an d 1 .1 7 Â ±0 .0 6, resp ectiv ely . A fter c aptop ril ad min istra
tion, GFR and ERPF were 0.27 ±0.03 (p < 0.0005) and
1.0 5 Â ±0 .0 9 (p < 0 .0 00 1 ), resp ectively (F ig . 1 ). T he p ercen t
decrease in GFR and ERPF-induced by captopril in the
group of animals treated with diuretic and in the group
w ith ou t d iu re tic (p rio r to c ap to pril a dm in istra tio n) w as
no t s ign if icant ly d if fe rent .
C h ro n ic Diu re tic E ffe c t o n G FR an d E R PF
In the 1K1C group, GFR after 1 wk of peritoneal
injection of HCTZ was 0.33 ±0.03 (s.e.). Captopril ad
AcuteStudies
odel
Procedure
Con t r o lS t u d i e s
Model
740
The Journal of Nuclear Medicine •ol. 33 •o. 5 •ay1992
METhODS
Male Sprague Dawley r at s we igh ing 280—300g were s tud ied
1-2 w k after the left renal artery w as clam ped. Renal artery
ste no sis w as p ro du ced by clam pin g th e left ren al artery w ith
p oly eth yle ne tu bin g (PE 5 0). T wo m illim ete r le ng th s o f tu bin g
w ere c ut lo ng itu din ally a nd p la ce d o ve r th e m ain re na l a rte ry .
T he r ats wer ema in ta in ed on a norma l d ie t w ith la bo ra to ry puri na
chow and provided with w ater ad libitum . At the tim e of the
r en al c le ar an ce s tudy , c ath ete rs we re p la ce d i n t he le ft a nd r ig ht
u re te r (PE 1 0 s ila stic tu bin g), femo ra l v ein a nd a rte ry (PE 5 0).
B lo od p re ss ure w as re co rd ed o n a Hew le tt P acka rd 7 8205D
recorder using a fem oral artery catheter. T he m ean of three
meas ur ements dur in g e ach time per io d wa s u se d f or th e a na ly sis .
T he in te rv en tio ns u se d a re summariz ed in T ab le 1 .
A c u t e S t u d i e s
Con tr ol r en al c le ar an ce wa s d et ermin ed 1 wk a fte r ope ra tio n
usi ng cont inuous i nfus ion in t he an ima ls t ha t r ece ived furosemide
o r h yd ro ch lo ro th ia zid e (HCT Z). A nim als tre ate d w ith c hlo ro
t hi az id e d id not a cu te ly h av e con tro l c le ar an ce s p er fo rmed. Fol
l ow ing thr ee cont ro l pe ri ods, r at s w i th 1K1C recei ved furosemide
intravenously, 0.15 mg (Group 1, n = 10) or HCTZ 1.5 mg
(G roup 2, n = 9) 15 m m prior to A CE . C hiorothiazide (C TZ )
wasadminister edas 1 .0mg in 10ml ofdrink ing waterovern igh t
(G roup 3, n = 8). C aptopnl (1.3—1.7m g per 100 g B WT ) w as
i nj ec te d in tr av enou sl y a nd b lood p re ss ur e was meas ur ed . When
blood pressure was s tabil ized, three pos t-captopr il c learances were
done.
Chroni c S tud ie s
For the chronic experim ent, 1K1C (G roup 4, n = 11) and
2 K1 C (G ro up 5 , n = 10 ) rats receiv ed 4 m g H CT Z b y p erito nea l
i nj ec tio n d aily f or 7 †”10ays p rio r to ACE .
G FR a n d E R P FMe a s u re m e n t
A fte r th e ra ts w ere awa ke , n orm al sa lin e w as in fu se d in to th e
fem oral vein at a rate of 1.5 m i/hr for 2K1C or 1.0 m i/hr for
1K1C r at s u si ng a SAGEau toma ti c i nf us ion pump . GFR and
T A B L E I
Study Design
1 K i C
Controlfollowedby iv. furosemideGpl
Controlfollowedby HC TZ Gp2
CTZ withoutcontrol Gp3
Eachof theabovefollowedbyi.v.captopnl
Chronicstudies
Model 1K1C
HC TZ7 —1day peritonealnjectionfollowed
by iv. cap topnl (Gp4)
2K1C
HC TZ7-1 0 day peritonealnjectionfollowed
by u.v.captopnl Gp5
1KiC
COntrOlfol lowed by i .v . captopn l (Gp6)
2K1C
Controlfollowedby i.v.captopnl (Gp6)
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A cute Diuretic Therapy 1K1C
No Diu re t ic Fu ro s em id e HCTZ CTZ
Ch r o n ic D iu r e tic T h e r a p y
n=10 n=11
I SE.
0 D iu re tic
0 D iu re ti c
Ca@I
I SE.
0 C on tro l
U D iu re tic
0 D iu re t ic
Captopri l
E
E
0
C
E
E
E
F IGURE I. GFRandER PFr e s p on s eo a c u t ed i u r e t ich e r ap y
and captopril is illustrate d for the 1 Ki C ra t. T he responses of
GFR and ERPFto acute d iu ret ic therapy alone were no t s ign if i
cant. The addit ionof captopnldecreasedGFR significant lywhen
comparedwith baselineand with diuret ic therapyalone.
ministration decreased GFR to 0. 18 ±0.04 (p < 0.007).
ER PF decreased from 1.20 Â ±O .07d to 0.79 Â ±0.16 p <
0 .0 2 F ig . 2 .
Afte r 1wk o fp erito ne al in je cti on o fHCTZ , th e c lamped
kidney in the 2K1C animals decreased GFR from 0.21 ±
0 .0 3 t o 0 . 1 1 ±0 .0 3 p < 0 .0 0 5 ). T h e E RPF f e ll f ro m 0 .7 0
±0.07 to 0.47 ±0. 13 (ns). The GFR in the contralateral
kidney prior to captopril adm inistration w as 0.34 Â ±0.02
and after captopril it was 0.35 ±0.02 (ns). The ERPF
in creased sig nifican tly fro m 0 .9 9 Â ±0 .0 5 to 1 .1 6 Â ±0 .0 9 (p
< 0.0 1) (Fig. 2).
In the 2 K1C con trol group of anim als, con trol G FR in
the clamped kidney was 0.20 ±0.02 (n = 19) and ERPF
was 0.61 ±0.06. A fter captopril treatm ent, GFR (0.10 ±
0.02, p < 0.0005 and ERPF 0.37 ±0.07, p < 0.00004
d ec re as ed sig nific an tly . C ap to prii d id n ot a ffe ct c on tra la t
eral kidney G FR significantly but was associated w ith an
increase in ERPF that was significant (p < 0.001). The
p erc en ta ge d ec re as e o fGFR and ERPF cau sed b y c ap to pril
in the group of animals treated with diuretics prior to
c ap to pn l w as n ot s ig nific an tly d iffe re nt from t he chang es
in animals that did not receive diuretic treatment. The
chang es observed in renal fu nction in all of these g roups
of anim als are sum ma rized in T able 2.
F IGURE2 . GFRa n dERPFre s p o n s eo c h ro n ic i u re t ich e r
apy fo llowed b y c ap to pril i n th e 1K i C and 2K1C ra ts is s hown.
GFR re s p o n s e sin t h e 1 K i C a n d in t h e c la m p e dk id n e yo f 2 K 1C
we r e s ig n if ic a n t , u t n o t i n t h e n o rm a lk i d n e y .ERP F in t h e 1K i C
decreasedsign if ican tly,bu t no t in the c lampedk idneyo f 2K1C.
ERP Fin the normalkidneyof 2K1C increasedsignificant ly.Single
as te risk ind ica tes2p < 0.05 and doubleas te risk ind ica tes2p <
0.01.
B l o o d P r e s s u r e
Blood pressure response in each group is shown in
Figures 3 and 4. The acute diuretic-treated 1K1C anim als
d id n ot d ec re as e b lo od p re ssu re sig nific an tly , b ut b lo od
pressure decreased significantly after ACE (Fig. 3).
Chro nic d iu re tic tre atm en t d ec re ase d b lo od p re ssu re sig
nificantly in bo th the 1K 1C and 2K 1C group s (F ig. 4). In
th e g ro up o f a nim als n ot re ce iv in g d iu re tic s p rio r to c ap
topril, blood pressure (m mHg) reduction after captopril
between the 2K1C and 1K1C groups were significantly
different. Blood pressure in the 2K1C group decreased by
â €”27 .8Â ±3 .5 s .e .) m m Hg , a n d in th e 1K 1C g ro up , it
decreased by †”15 .5  ±21 .2. A fter ch ro nic d iu retic treat
m ent, the blood p ressure in 2K 1C and 1K 1C rats w ere not
significantly different.
DISCUSS ION
Since diuretic therapy is used w idely in hypertensive
patients, its potential influence on captopnl renography is
of great im portance. The use of a diuretic in addition to
captopril m ay play a role in the developm ent of captopnl
Cap toprilDu ringDiureticThe rapy•eeand Blau fox
741
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2K1C
G FR E R P F G FR
G ro up R x N K C 1K N K C 1K C 1K1K1C E R P F
C 1K
1
n =19 n=1O n=9 n =8
TABLE2
E ffe c t s o f D iu re t ic s a n d Ca p to p ril R e n a l C le a ra n c e
Control0 .34
±0. 0 31
.25  ±.0AcuteFuro0.30±0.021.06±0.06Furo
ACEI0.23
±O.O 2@ 1
.2 1 Â ±.062Con tro l
H CTZ
HCTZ ACEI0.38±0.05
0 .38±0 .05
0 .27 ±O.04@ 1.17±0 .13
1.1 5Â ±0.1 3
1 . 0 9±. 143CTZ ,
Acu t e
CTZ ACEI0.39
 ±0 .0 2
0 . 2 5± . 06*1
. 22 ±0 .05
0 . 9 7±. 024HCTZ ,
Chron i c
H CTZ+ ACE I0 . 33
±0.03
0 .1 8 ±0 .0 41
.20 ±0.0 7
0.79 Â ±.16 5HCTZ,
Chronic
HCTZ ACEI0.34
 ±0 .0 2
0.35 ±0.020 .21
±0 .0 3
0.11 ±0.0 3*0.99
±0.05
1.16 ±0.0 90 .70
±0.07
0 . 4 7±.136Con t ro l
C on t + A CE I0 .3 8
 ±0 .0 2
0.37 ±0.020 .20
±0.02
0 .10 ±O .02@0 .95
±0.05
1.12 ±0.06 0 .61
 ±0 .0 6
0 .37 ±O.O7@ 0.36
 ±0 .0 2
0 .27 ±O [email protected]
 ±0 .0 6
1.05 Â ±.09 2p@
8/18/2019 J Nucl Med-1992-Lee-739-43
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in all patients except patients with low renin (12). Some
patients with RAS developed positive sodium balance,
whil e o th er s developed negat iv e sod ium bal ance , a lt hough
all p atien ts ex perien ced b lo od p ressu re red uctio n (4 ,1 2).
In 1K 1C an d 2K 1C rats w ith R VH , c aptopril increases
urinary sodium excretio n and plasm a-renin le vels and
re su lts in d ec re ase d b lo od p re ssu re (1 5,1 6). T he d ep en d
ency of autoregulation of G FR on the renin angiotensin
system in these anim als is m ost m arked during sodium
d ep le tio n (7 ). U nd er c on ditio ns o f so dium d ep le tio n a nd
increased renin, inhibition of ACE is expected to disturb
autoregulation. W hen the renin angiotensin system is
blocked, sodium and w ater retention m ay play a role in
the pa thogenesis of 1K 1C hypertension but not in tha t of
2K1C (1 7).
T he k id ne ys w ith RA S in b oth 1K 1C a nd 2K1C a nim als
h av e a low p erfu sio n p re ss ure , th ere fo re th ey te nd to re ta in
sodium . H ow ever, in 1K 1C anim als, hypertension w as
a sso cia te d w ith a p ro gre ssiv e p os itiv e so dium b ala nc e,
while 2K1C anima ls d ev elo ped a p ro gr es siv e n eg ativ e s o
d ium b ala nc e, p ro ba bly d ue to th e so dium e xc re tio n from
th e c on tra la te ra l k id ne y (1 7 ). In 1K1C a nim als, so dium
re te ntio n con ti nu es u nt il re gu la tin g mech an isms d ev elo p
a new equilibrium of sodium ba lance. T he rise in central
a rte ria l p re ss ur e is a n importa nt fa cto r in th e equ il ib rium ,
since it tends to raise the pressure in the renal artery distal
to th e s te no sis . T he d ep en dency o fa uto re gu la tio n o f GFR
o n th e R A S is m o s t m a rk e d d urin g s od iu m de ple tio n 7 .
The GFR is usually m aintained in the sodium replete
state, but m ild sodium and w ater depletion can im pair
r enal function .
In patients w ith severe bilateral R AS , renal function
d ete rio ra te s (1 ,1 8) d urin g th e c ombin atio n o f c ap to pril
and diu retic treatm ent but not w ith c aptopril alone. T he
dependency ofautoregulation ofGFR on the RA S is m ore
m ark ed durin g a com bination of captopril and diuretic
treatment.
I n th e p re se nt s tu dy , th e a cu te in tra veno us adm in is tra
tion of furosemide or HCTZ in 1K1C rats did not change
G FR or E RPF significantly. A CE adm inistered after the
d iu re tic d ec re ase d GFR s ig nific an tly , w hile c ap to pril g iv en
to a nima ls a dm in is te re d CTZ in d rin kin g wate r o ve rn ig ht
p rio r to ACE d ec re as ed GFR s ig nific an tly b ut n ot ERPF .
C ap to pril ad min istratio n to ra ts receiv in g H CT Z in trap er
itone ally for 7-10 d ays decre ased bo th G FR and E RP F in
iKlC rats, while in 2K1C rats it decreased GFR in the
clam ped kidney but not in the contralateral kidney. E RP F
in the 2K1C group did not change in the clamped kidney
but i nc reas ed s igni fi cant ly i n t he con tr al at er al k idney a ft er
A C E . F or con tr ol 1K 1 C r at s t hat d id n ot r ecei ve d iu r et ics
prior to ACE , there was a decrease in both GFR and
E RPF af ter A CE . B ot h G FR and E RPF decr eased si gni f
icantly after A CE in the clam ped k idney in the co ntrol
2K 1C rats. In the contralatera l kidney in th ese an im als,
G FR did not change and ER PF increased significantly.
T he e ffe cts o f d iu re tic s o n re na l fu nc tio n in a nim als w ith
RAS a re v aria ble . T he c on se qu en ce s o f A CE o n G FR a re
sim ila r w ith o r w ith ou t d iu re tic s. T he se d ata s ug ge st th at
d iu re tic th er ap y may not s ig nific an tly in te rf ere w ith ACE
evaluation of R VH .
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1992;33:739-743.J Nucl Med.
Hyo Bok Lee and M. Donald Blaufox Renal Functional Response to Captopril During Diuretic Therapy
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