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重度高血压会引发肾脏自身调节功能紊乱。

Severe hypertension induces disturbances of renal autoregulation.

作者信息

Almeida J B, Saragoça M A, Tavares A, Cezareti M L, Draibe S A, Ramos O L

机构信息

Hypertension-Nephrology Division, Escola Paulista de Medicina, São Paulo, Brazil.

出版信息

Hypertension. 1992 Feb;19(2 Suppl):II279-83. doi: 10.1161/01.hyp.19.2_suppl.ii279.

Abstract

To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n = 10) with those of a group of patients with severe hypertension (n = 10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6 +/- 8.3% and -44.7 +/- 6.8%, respectively; p less than 0.01 for both) but not in those with moderate hypertension (+4.9 +/- 9.1% and +6.2 +/- 13.3%, respectively; NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow.

摘要

为研究高血压的严重程度是否与肾血流自动调节及肾小球滤过的紊乱相关,我们比较了一组中度原发性高血压患者(n = 10)和一组重度高血压患者(n = 10)对急性血压降低的肾血流动力学及功能反应。通过逐步输注硝普钠将血压降至正常水平,并测定有效肾血流量(通过131I - 马尿酸)、肾小球滤过率(通过内生肌酐清除率)及滤过分数。急性血压正常化后,重度高血压患者的有效肾血流量和肾小球滤过率显著降低(分别为 - 41.6 ± 8.3%和 - 44.7 ± 6.8%;两者p均小于0.01),而中度高血压患者则未降低(分别为 + 4.9 ± 9.1%和 + 6.2 ± 13.3%;无显著性差异)。两组的滤过分数均保持不变。这些结果表明,重度而非中度原发性高血压患者在急性血压降低期间,由于血管舒张受损,肾自动调节曲线下限向右移位,以维持足够的肾血流量。这种损害可能是由于肾小球前血管的解剖或功能缺陷,或两者皆有。此外,在这些情况下无法维持足够的肾小球滤过表明,重度高血压患者在面对肾小球血流量减少时,调节肾小球后血管舒缩张力的能力也受损。

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