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肾小球出球小动脉收缩:高血压中一种可能的肾内血流动力学缺陷。

Efferent glomerular arteriolar constriction: a possible intrarenal hemodynamic defect in hypertension.

作者信息

Frohlich E D

机构信息

Alton Ochsner Medical Foundation, New Orleans, Louisiana 70121.

出版信息

Am J Med Sci. 1988 Apr;295(4):409-13. doi: 10.1097/00000441-198804000-00032.

Abstract

A variety of mechanisms involving the kidney subserve the control of arterial pressure and the development and maintenance of hypertension. The precise and direct delineation of intrarenal hemodynamic mechanisms has been possible only by micropuncture techniques. Since these methods can be used only in the anesthetized animal, intrarenal hemodynamic assessment in conscious intact experimental animals or patients with essential hypertension must be indirect. Using indirect methods, calculated pressures in our laboratory have demonstrated differences in intrarenal hemodynamics between SHR and normotensive WKY rats, notably enhanced responsiveness of the efferent arteriole to alpha adrenergic agonist stimulation. When the calcium antagonist diltiazem was administered to the SHR or to patients with essential hypertension, it effected an increased renal blood flow and a well-maintained glomerular filtration rate without hyperfiltration. These indirect data suggest that there may be an efferent arteriolar abnormality in genetically mediated hypertension that may be reversed with certain calcium antagonists.

摘要

涉及肾脏的多种机制有助于控制动脉血压以及高血压的发生和维持。只有通过微穿刺技术才能精确而直接地描绘肾内血流动力学机制。由于这些方法仅能用于麻醉动物,因此对清醒的完整实验动物或原发性高血压患者进行肾内血流动力学评估必须采用间接方法。运用间接方法,我们实验室计算出的压力表明,自发性高血压大鼠(SHR)和血压正常的WKY大鼠在肾内血流动力学方面存在差异,尤其是出球小动脉对α肾上腺素能激动剂刺激的反应性增强。当给SHR或原发性高血压患者施用钙拮抗剂地尔硫䓬时,肾血流量增加,肾小球滤过率得以良好维持且无超滤现象。这些间接数据表明,在基因介导的高血压中可能存在出球小动脉异常,而某些钙拮抗剂可能会使其逆转。

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