Endocrinology, Vol 120, 1384-1390, Copyright © 1987 by Endocrine Society

ARTICLES

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.

This article has been cited by other articles:

				T. Yamamoto, T. Nakagawa, H. Suzuki, N. Ohashi, H. Fukasawa, Y. Fujigaki, A. Kato, Y. Nakamura, F. Suzuki, and A. Hishida Urinary Angiotensinogen as a Marker of Intrarenal Angiotensin II Activity Associated with Deterioration of Renal Function in Patients with Chronic Kidney Disease J. Am. Soc. Nephrol., May 1, 2007; 18(5): 1558 - 1565. [Abstract] [Full Text] [PDF]

				M. Azizi, E. Ezan, L. Nicolet, J.-M. Grognet, and J. Menard High Plasma Level of N-Acetyl-Seryl-Aspartyl-Lysyl-Proline : A New Marker of Chronic Angiotensin-Converting Enzyme Inhibition Hypertension, November 1, 1997; 30(5): 1015 - 1019. [Abstract] [Full Text]

				P. Corvol and X. Jeunemaitre Molecular Genetics of Human Hypertension: Role of Angiotensinogen Endocr. Rev., October 1, 1997; 18(5): 662 - 677. [Abstract] [Full Text]