1. The purpose of the present investigation was to determine whether a
n abnormality of the renal papillary circulation is present in a well-
established model of cirrhosis without ascites (carbon tetrachloride/p
henobarbital). 2. Compared with the control animals, cirrhotic rats sh
owed a reduced diuretic (61.0+/-5.1 versus 18.0+/-2.5%) and natriureti
c (67.8+/-8.3 versus 29.6+/-3.6%) response to a volume expansion (3% b
ody weight infusion of 0.9% NaCl). The volume expansion-induced increa
se in renal interstitial hydrostatic pressure was also blunted in the
cirrhotic rats (control 9.3+/-0.9 versus cirrhotic 6.1+/-1.0 mmHg) and
there were no differences in mean arterial blood pressure, renal bloo
d flow or glomerular filtration rate between control and cirrhotic ani
mals. 3. Papillary plasma flow was determined by the I-125-albumin acc
umulation technique and expressed as ml min-1 100 g-1. In the basal st
ate, papillary plasma flow was significantly lower in cirrhotic rats (
59.1+/-4.4, n=9) than in the control animals (81.8+/-6.9, n=9). An iso
tonic saline expansion similar to the one described above significantl
y increased papillary plasma flow in control rats (108.4+/-9.1, n = 7)
but did not change it in cirrhotic rats (60.2+/-4.9, n=6). 4. Our res
ults indicate the existence of a selective alteration in the renal pap
illary circulation in cirrhotic rats, both in the basal state and afte
r a well-established vasodilatory stimulus. The reduced papillary plas
ma flow of the cirrhotic animals, probably mediated through changes in
renal interstitial hydrostatic pressure, may participate in the sodiu
m and water retention that precedes the development of ascites and may
be an important mechanism mediating the blunted renal response to ext
racellular volume expansion.