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库欣综合征高血压的血管紧张素生成机制的证据。

Evidence for an angiotensinogenic mechanism of the hypertension of Cushing's syndrome.

作者信息

Dalakos T G, Elias A N, Anderson G H, Streeten D H, Schroeder E T

出版信息

J Clin Endocrinol Metab. 1978 Jan;46(1):114-8. doi: 10.1210/jcem-46-1-114.

Abstract

The blood pressure response to the angiotensin II analog 1-sar-8-ala-angiotensin II, or saralasin, was studied in five patients with clinical and laboratory evidence of Cushing's syndrome. Plasma renin activity, plasma renin substrate, and plasma renin concentration were measured in all five patients. The renin system and the response to saralasin were measured after furosemide administration. Plasma aldosterone was measured after infusion of 2 liters normal saline. All patients studied showed a hypotensive response to saralasin, the mean BP changing from 163/108 mm Hg to 130/85 mm Hg (P less than 0.02). There was a significant elevation of the plasma renin activity and plasma renin concentration in the patients compared to normal subjects, although plasma renin substrate was not significantly different from normal values. There was normal suppression of plasma aldosterone after the infusion of 0.9% saline. The findings indicate that the hypertension of these patients with Cushing's syndrome was mediated in large part by angiotensin II.

摘要

对5例有库欣综合征临床及实验室证据的患者,研究了其对血管紧张素II类似物1 - 肌氨酸 - 8 - 丙氨酸血管紧张素II(即沙拉新)的血压反应。测定了所有5例患者的血浆肾素活性、血浆肾素底物及血浆肾素浓度。在给予速尿后测定肾素系统及对沙拉新的反应。在输注2升生理盐水后测定血浆醛固酮。所有研究患者对沙拉新均表现出降压反应,平均血压从163/108 mmHg变为130/85 mmHg(P<0.02)。与正常受试者相比,患者的血浆肾素活性及血浆肾素浓度显著升高,尽管血浆肾素底物与正常值无显著差异。输注0.9%生理盐水后,血浆醛固酮受到正常抑制。这些发现表明,这些库欣综合征患者的高血压在很大程度上是由血管紧张素II介导的。

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