Candesartan cilexetil and renal hemodynamics in hypertensive patients

被引:19
|
作者
Fridman, K
Wysocki, M
Friberg, P
Andersson, OK
机构
[1] Sahlgrens Univ Hosp, Dept Internal Med, Gothenburg, Sweden
[2] Sahlgrens Univ Hosp, Dept Clin Physiol, Gothenburg, Sweden
关键词
angiotensin II receptor-blocker; candesartan cilexetil; hypertension; renal plasma flow; renal vascular resistance;
D O I
10.1016/S0895-7061(00)00302-2
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
This randomized, double-blind, placebo-controlled crossover study evaluated the effects of the angiotensin II type 1 (AT(1))-receptor blocker candesartan cilexetil on renal blood perfusion and glomerular filtration in patients with primary hypertension with diastolic blood pressure of 100 to 114 mm Hg. After a 4-week placebo run-in period, patients were randomized to receive either 16 mg candesartan cilexetil or placebo once daily for 6 weeks, after which they were switched to the alternative treatment. At the end of each period, 24 h after the last dose, renal assessments were made and the plasma renin activity, plasma concentrations of angiotensin II, aldosterone, and catecholamines were measured. Compared with placebo, candesartan cilexetil significantly reduced mean arterial pressure, by 8 mm Hg (95% confidence interval [CI], 3;12). Renal vascular resistance was significantly reduced by 0.03 mm Hg/mL min(-1) (95% CI, 0.01;0.06). There was a small nonsignificant increase in renal plasma now. The filtration fraction fell slightly from 0.24 to 0.22 (95% CI, -0.00, 0.04). As expected, angiotensin II concentrations and plasma renin activity were increased and the aldosterone concentrations were reduced. Catecholamine concentrations were unaffected. In conclusion, 6 weeks' treatment with 16 mg candesartan cilexetil once daily induced a reduction of renal vascular resistance and a trend toward increased renal plasma now despite a reduction in mean arterial pressure. Because the glomerular filtration rate was maintained the filtration fraction was reduced, indicating a decreased glomerular capillary pressure. Am J Hypertens 2000;13:1045-1048 (C) 2000 American Journal of Hypertension, Ltd.
引用
收藏
页码:1045 / 1048
页数:4
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