Norman R A, Galloway P G, Dzielak D J, Huang M
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
J Hypertens. 1988 May;6(5):397-403.
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.
在斯普拉格-道利大鼠中研究了肾素-血管紧张素系统和免疫系统对肾梗死性高血压病因的影响。通过结扎和切断左肾动脉三个分支中的两个分支造成部分肾梗死。右肾保持完整。肾梗死导致稳定高血压的快速发展。梗死后一周，血浆肾素活性（PRA）增加了三倍多。然而，梗死后4周PRA恢复到对照水平。用环磷酰胺进行慢性免疫抑制治疗最多只能减轻与这种短暂肾素升高相关的肾梗死性高血压的发展。然而，环磷酰胺可防止高血压后期的维持阶段，并且还可完全逆转已确立的梗死性高血压。肾素-血管紧张素系统的激活在部分肾梗死性高血压的发病中起作用，但维持高血压需要完整的免疫系统。据推测，针对肾组织的免疫反应维持肾梗死性高血压。
