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Sodium, angiotensin II, blood pressure, and cardiac hypertrophy.
Morgan, T O; Aubert, J F; Wang, Q.
Affiliation
  • Morgan TO; Department of Physiology, University of Melbourne, Parkville, Australia. t.morgan@physiology.unimelb.edu.au
Kidney Int Suppl ; 67: S213-5, 1998 Sep.
Article in En | MEDLINE | ID: mdl-9736294
Blood pressure (BP) in rats was elevated intermittently by i.p. injections of angiotensin II (Ang II; 200 microg/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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Collection: 01-internacional Database: MEDLINE Main subject: Sodium / Blood Pressure / Angiotensin II / Hypertrophy, Left Ventricular / Kidney Limits: Animals Language: En Journal: Kidney Int Suppl Year: 1998 Document type: Article Affiliation country: Australia Country of publication: United States
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Collection: 01-internacional Database: MEDLINE Main subject: Sodium / Blood Pressure / Angiotensin II / Hypertrophy, Left Ventricular / Kidney Limits: Animals Language: En Journal: Kidney Int Suppl Year: 1998 Document type: Article Affiliation country: Australia Country of publication: United States