Mechanisms of partial renal infarct hypertension
作者:
Roger,
Norman Paula,
Galloway David,
Dzielak Min,
期刊:
Journal of Hypertension
(OVID Available online 1988)
卷期:
Volume 6,
issue 5
页码: 397-404
ISSN:0263-6352
年代: 1988
出版商: OVID
关键词: Hypertension;immunosuppression;renal infarction;renin-angiotensin system
数据来源: OVID
摘要:
Contributions of both the renin-angiotensin and immune systems to the aetiology of renal infarct hypertension were examined in Sprague-Dawley rats. Partial renal infarction was produced by ligating and sectioning two out of three branches of the left renal artery. The right kidney remained intact. Renal infarction resulted in rapid development of stable hypertension. One week following infarction, the plasma renin activity.(PRA) increased more than threefold. However, PRA returned to control levels 4 weeks after infarction. Chronic immunosuppressive therapy with cyclophosphamide at most only attenuated the development of renal infarct hypertension associated with this transient renin elevation. However, cyclophosphamide prevented the later maintenance phase of the hypertension, and could also completely reverse established infarct hypertension. Activation of the renin-angiotensin system plays a role in the onset of partial renal infarct hypertension, but an intact immune system is required for maintenance of the hypertension. It is hypothesized that immunological reactions against renal tissue maintain renal infarct hypertension.
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