J Nucl Med-1992-Lee-739-43

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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 â€”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 7â€”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;33:739â€”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 â€¢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

by Indonesia: J of Nuclear Medicine Sponsored on April 4, 2016. For personal use only. jnm.snmjournals.orgDownloaded from

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ERPF weremeasuredwhen urine f lowwas s tab le .Technetium

99m-DTPA(50 @iCi)nd [â€˜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 [â€ ˜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 €˜@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 Â±0.03 (s.e.) and

0.30 Â±0.02 (ns), respectively. The GFR of control and

HCTZ -tre ate d anima ls w ere 0 .3 8 Â±0 .0 5 and 0 .3 8 Â±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 Â±0. 13 and 1. 15 Â±

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 Â±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

Â±0.02 to 0.25 Â±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 Â±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 Â±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 Â±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 â€¢ol. 33 â€¢o. 5 â€¢ay1992

METhODS

Male Sprague Dawley r at s we igh ing 280â€”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 (1.3â€”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 â€ ”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 â€”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 Â±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 Â±

0 .0 3 t o 0 . 1 1 Â±0 .0 3 p < 0 .0 0 5 ). T h e E RPF f e ll f ro m 0 .7 0

Â±0.07 to 0.47 Â±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 Â±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 Â±0.02 (n = 19) and ERPF

was 0.61 Â±0.06. A fter captopril treatm ent, GFR (0.10 Â±

0.02, p < 0.0005 and ERPF 0.37 Â±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 â€ ”15 .5 Â ±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 rapyâ€¢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

Â±0. 0 31

.25 Â ±.0AcuteFuro0.30Â±0.021.06Â±0.06Furo

ACEI0.23

Â±O.O 2@ 1

.2 1 Â ±.062Con tro l

H CTZ

HCTZ ACEI0.38Â±0.05

0 .38Â±0 .05

0 .27 Â±O.04@ 1.17Â±0 .13

1.1 5Â ±0.1 3

1 . 0 9Â±. 143CTZ ,

Acu t e

CTZ ACEI0.39

Â ±0 .0 2

0 . 2 5Â± . 06*1

. 22 Â±0 .05

0 . 9 7Â±. 024HCTZ ,

Chron i c

H CTZ+ ACE I0 . 33

Â±0.03

0 .1 8 Â±0 .0 41

.20 Â±0.0 7

0.79 Â ±.16 5HCTZ,

Chronic

HCTZ ACEI0.34

Â ±0 .0 2

0.35 Â±0.020 .21

Â±0 .0 3

0.11 Â±0.0 3*0.99

Â±0.05

1.16 Â±0.0 90 .70

Â±0.07

0 . 4 7Â±.136Con t ro l

C on t + A CE I0 .3 8

Â ±0 .0 2

0.37 Â±0.020 .20

Â±0.02

0 .10 Â±O .02@0 .95

Â±0.05

1.12 Â±0.06 0 .61

Â ±0 .0 6

0 .37 Â±O.O7@ 0.36

Â ±0 .0 2

0 .27 Â±O [email protected]

Â ±0 .0 6

1.05 Â ±.09 2p@

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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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CaptopnlDunngDiureticTherapy â€¢ee and Blaufox

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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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