Affiliation:
1. From Duke University and Durham Veterans Affairs Medical Centers, Durham, NC (M.I.O., C.F.B., T.M.C.), and the Department of Pathology, University of North Carolina, Chapel Hill (O.S.).
Abstract
Abstract
—To examine the role of the angiotensin II (AT)
1A
receptor in the regulation of blood pressure and sodium balance, we measured systolic blood pressure responses in AT
1A
receptor–deficient (
Agtr1a
−/−) and wild-type (
Agtr1a
+/+) mice while dietary sodium content was systematically altered. On a 0.4% sodium diet, systolic blood pressures were significantly lower in
Agtr1a
−/− than in +/+ mice. In
Agtr1a
+/+ mice, changing dietary sodium content did not affect blood pressure. In contrast, when
Agtr1a
−/− mice were fed a high-salt diet (6% NaCl), their systolic blood pressures increased significantly from 79±4 to 94±4 mm Hg (
P
<0.006). The low blood pressures of
Agtr1a
−/− mice decreased further while on a low-salt diet from 82±3 to 69±3 mm Hg (
P
<0.03). On the high-salt diet, urinary sodium excretion increased to similar levels in
Agtr1a
+/+ and −/− mice. Although urinary sodium excretion was substantially reduced in both groups during the low-salt diet, cumulative sodium balances became negative in
Agtr1a
−/− mice despite a 6-fold increase in urinary aldosterone. We infer, therefore, that the reduced blood pressures in
Agtr1a
−/− mice on a normal diet are caused by depletion of sodium and extracellular volume. Their “sodium sensitivity” suggests a critical role for renal AT
1A
receptors to modulate sodium handling.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Cited by
96 articles.
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