Artigo Acesso aberto Revisado por pares

Sodium, angiotensin II, blood pressure, and cardiac hypertrophy

1998; Elsevier BV; Volume: 54; Linguagem: Inglês

10.1046/j.1523-1755.1998.06751.x

ISSN

1523-1755

Autores

Trefor Morgan, Jean-Francois Aubert, Qing Wang,

Tópico(s)

Renal function and acid-base balance

Resumo

Sodium, angiotensin II, blood pressure, and cardiac hypertrophy. Blood pressure (BP) in rats was elevated intermittently by i.p. injections of angiotensin II (Ang II; 200 μg/kg), and the effect on cardiac index was determined. The BP response was assessed in selected rats by telemetry. Elevation of BP between 8:00 and 12:00 produced cardiac enlargement similar to that produced by continuous Ang II infusion, and the response correlated better with the acute BP elevation than with 24-hour cardiac work. A high-sodium diet also increased left-ventricular hypertrophy (LVH) without a major effect on BP. The addition of Ang II intensified this response. A low-sodium diet had no significant effect on BP or on cardiac size, but prevented the cardiac hypertrophy produced by Ang II without altering the BP response. These results suggest that acute BP elevation, probably working through increased wall tension, is a more potent stimulus for cardiac hypertrophy than 24-hour workload. The sodium intake of the rat plays an important role influencing the cardiac but not the BP response to Ang II. These results infer that it is important to avoid episodes of acute BP elevation.

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