Endocrinology, Vol 120, 1384-1390, Copyright © 1987 by Endocrine Society
Liver angiotensinogen synthesis and release during captopril treatment in sodium-depleted rats
HN Jaramillo, MP Sambhi, J Bouhnik, P Corvol and J Menard
In vivo generation of angiotensins depends upon both plasma renin and
angiotensinogen concentrations. Those factors which may influence hepatic
angiotensinogen synthesis and release were examined. We have evaluated in
vivo the effects of converting enzyme inhibition on several plasma
renin-angiotensin system components, and, using an in vitro preparation of
liver slices, we also investigated the effects of converting enzyme
inhibition on the synthesis and release of hepatic angiotensinogen.
Angiotensinogen concentrations were determined by two different methods.
The first was an indirect enzymatic assay which measures the amount of
angiotensin I liberated from plasma by an excess of renin. The second was a
direct RIA that measures both angiotensinogen and its inactive residue the
des-angiotensin I- angiotensinogen. The difference between the methods
represents the circulating levels of des-angiotensin I-angiotensinogen.
Captopril administration in sodium-depleted rats increased plasma
concentrations of renin, des-angiotensin I-angiotensinogen, and angiotensin
I and decreased plasma angiotensinogen concentration measured by both
methods. Plasma des-angiotensin I-angiotensinogen was significantly
correlated to plasma renin concentration, which suggests an increase in the
consumption of angiotensinogen when the renin secretion is extremely
increased. The angiotensinogen liver content and in vitro angiotensinogen
release were decreased in sodium-depleted rats treated with a converting
enzyme inhibitor, and these parameters were negatively correlated to in
vivo plasma levels of renin, angiotensin I, and des-angiotensin
I-angiotensinogen. They were positively correlated to plasma
angiotensinogen concentration measured by the indirect assay. These data
suggest that captopril administration during sodium depletion has two
simultaneous effects: it increases angiotensinogen consumption and second,
decreases angiotensinogen production and release.
