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非少尿型肾衰竭中的高血压调节异常及其钙通道阻滞剂的改善作用

Hypertensive dysregulation and its modification by calcium channel blockade in nonoliguric renal failure.

作者信息

Weidmann P, Schohn D, Gnädinger M P, Bürgisser E, Ferrier C, Jahn H

机构信息

Medizinische Poliklinik, University of Bern, Switzerland.

出版信息

Am J Nephrol. 1989;9(4):269-78. doi: 10.1159/000167980.

DOI:10.1159/000167980
PMID:2683789
Abstract

UNLABELLED

To investigate the pathogenetic constellation and its modification by calcium channel blockade in hypertension associated with chronic nonoliguric renal failure, blood pressure (BP), various pressor factors or correlates, cardiovascular responsiveness, and plasma atrial natriuretic peptide (ANP) were assessed in 15 hypertensive patients (serum creatinine 160-715 mumol/l) before and after 6 weeks of intervention with the agent nitrendipine. On placebo, these patients had a lower plasma angiotensin II (AngII) clearance and higher values of supine plasma AngII, aldosterone, norepinephrine (NE), and heart rate than healthy humans. Acute responses of BP to AngII and of heart rate to isoproterenol were blunted in the patients (p less than 0.05-0.001). Plasma ANP was elevated, correlated positively with systolic BP, and rose in response to NE pressor infusion (p less than 0.05-0.001). Exchangeable sodium and blood volume did not differ significantly from normal values. Nitrendipine reduced the cardiovascular responses to AngII, NE, and isoproterenol and lowered supine BP from 173/102 +/- 5/2 to 146/81 +/- 3/3 mm Hg and upright BP from 170/105 +/- 5/2 to 145/86 +/- 4/3 mm Hg (p less than 0.05-0.001); except for slightly increased plasma AngII, the levels of other endocrine variables, exchangeable sodium, blood volume, and creatinine clearance were not significantly modified.

CONCLUSIONS

Hypertension accompanying chronic nonoliguric renal impairment seems to be strongly AngII and probably also NE dependent. Circulating ANP levels are high in this setting. Calcium channel blockade with nitrendipine effectively reduces cardiovascular AngII and NE dependence and BP.

摘要

未标记

为研究慢性非少尿性肾衰竭相关高血压的发病机制及钙通道阻滞剂对其的影响,对15例高血压患者(血清肌酐160 - 715μmol/L)在使用尼群地平干预6周前后进行了血压(BP)、各种升压因子或相关因素、心血管反应性及血浆心房利钠肽(ANP)的评估。服用安慰剂时,这些患者的血浆血管紧张素II(AngII)清除率较低,仰卧位血浆AngII、醛固酮、去甲肾上腺素(NE)及心率值高于健康人。患者对AngII的血压急性反应及对异丙肾上腺素的心率急性反应减弱(p < 0.05 - 0.001)。血浆ANP升高,与收缩压呈正相关,且对NE升压输注有反应性升高(p < 0.05 - 0.001)。可交换钠和血容量与正常值无显著差异。尼群地平降低了对AngII、NE及异丙肾上腺素的心血管反应,使仰卧位血压从173/102±5/2降至146/81±3/3 mmHg,直立位血压从170/105±5/2降至145/86±4/3 mmHg(p < 0.05 - 0.001);除血浆AngII略有升高外,其他内分泌变量、可交换钠、血容量及肌酐清除率水平无显著改变。

结论

慢性非少尿性肾功能损害伴发的高血压似乎强烈依赖AngII,可能也依赖NE。在此情况下循环ANP水平较高。尼群地平进行钙通道阻滞可有效降低心血管对AngII和NE的依赖性及血压。

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