doi: 10.1161/01.HYP.0000016177.20565.A0
(Hypertension. 2002;39:1007.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
Effects of Dietary Sodium and Genetic Background on Angiotensinogen and Renin in Mouse
From the Department of Human Genetics, University of Utah Health Sciences Center (P.L., A.R., B.G., E.H., T.C., J.T., S.X., T.I., J-M.L.), Salt Lake City; University Claude Bernard Lyon I (P.L.), Lyon, France; Howard Hughes Medical Institute (E.H., T.C., G.P., J-M.L.), Department of Obstetrics and Gynecology (T.H., K.W.), and Department of Pathology (D.A.T.) University of Utah, Salt Lake City; and US Department of Veterans’ Affairs (D.A.T.), Salt Lake City, Utah.
Correspondence to Jean-Marc Lalouel, MD, DSc, Eccles Institute of Human Genetics, Eccles Building, sixth floor, University of Utah Health Sciences Center, Salt Lake City, Utah. E-mail jml{at}howard.genetics.utah.edu
Elements of a renin-angiotensin system expressed along the entire nephron, including angiotensinogen secreted by proximal tubule and renin expressed in connecting tubule, may participate in the regulation of sodium reabsorption at multiple sites of the nephron. The response of this tubular renin-angiotensin system to stepwise changes in dietary sodium was investigated in 2 mouse strains, the sodium-sensitive inbred C57BL/6 and the sodium-resistant CD1 outbred. Plasma angiotensinogen was not affected by sodium regimen, whereas plasma renin increased 2-fold under low sodium. In both strains, the variation in urinary parameters did not parallel the changes observed in plasma. Angiotensinogen and renin excretion were significantly higher under high sodium than under low sodium. Water deprivation, by contrast, induced significant activation in the tubular expression of angiotensinogen and renin. C57BL/6 exhibited significantly higher urinary excretion of angiotensinogen than did CD1 animals under both conditions of sodium intake. The extent to which these urinary parameters reflect systemic or tubular responses to challenges of sodium homeostasis may depend on the relative contribution of sodium restriction and volume depletion.
Key Words: angiotensinogen • renin • sodium • mouse • genetics • urine
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