Document Detail


Captopril, but not nifedipine, improves endothelium-dependent vasodilation in hypertensive patients.
MedLine Citation:
PMID:  9759984     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study aimed to investigate the influence of the angiotensin-converting enzyme (ACE)-inhibitor captopril and the Ca-antagonist nifedipine on endothelium-dependent vasodilation (EDV) in the forearm of hypertensive patients. Twenty-three middle-aged untreated hypertensive patients underwent evaluation of EDV and endothelium-independent vasodilation (EIDV) in the forearm, by means of local intra-arterial infusions of methacholine (MCh, evaluating EDV) and sodium-nitroprusside (SNP, evaluating EIDV), before and 1 h after intake of either captopril (25 mg) or nifedipine (10 mg) in a randomised, double-blind fashion. A matched normotensive control group was investigated at baseline conditions only. Five of the hypertensives were also evaluated after 3 months of treatment with captopril 25 mg twice daily in an open pilot study. First, the vasodilation induced by methacholine (MCh), but not SNP, was significantly attenuated in the hypertensive patients compared to the normotensive controls (P < 0.001 at MCh 4 microg/min). Second, although the two drugs induced a similar decline in blood pressure (BP) 1 h after administration (-11 to 10 mm Hg/-8 to 7 mm Hg), captopril significantly potentiated the vasodilator response to MCh (+32+/-13%, MCh 4 micr og/min, P < 0.01) but not SNP, while nifedipine did not significantly alter the response to either MCh or SNP. The improvement in vasodilator response to MCh induced by captopril was closely related to the reduction in BP (r = 0.72, P < 0.01). Third, in the pilot study, 3 months of captopril treatment induced a significant potentiation of the vasodilator response to MCh (+34+/-17%, MCh 4 microg/min, P < 0.05) in parallel with a significant BP reduction (-22+/-24/13+/-13 mm Hg, P < 0.05), while the response to SNP was unchanged. In conclusion, the present study confirmed that essential hypertension is associated with a defect in EDV. Furthermore, an improvement in EDV was seen in hypertensive patients shortly after administration of captopril, but not nifedipine. In addition, a significant beneficial effect on EDV was seen in a small pilot study during long-term treatment with captopril.
Authors:
J Millgård; A Hägg; M Sarabi; L Lind
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Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of human hypertension     Volume:  12     ISSN:  0950-9240     ISO Abbreviation:  J Hum Hypertens     Publication Date:  1998 Aug 
Date Detail:
Created Date:  1998-11-24     Completed Date:  1998-11-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8811625     Medline TA:  J Hum Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  511-6     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University Hospital of Uppsala, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Aged
Angiotensin-Converting Enzyme Inhibitors / pharmacology*,  therapeutic use
Arteries / physiopathology
Calcium Channel Blockers / pharmacology,  therapeutic use
Captopril / pharmacology*,  therapeutic use
Double-Blind Method
Endothelium, Vascular / drug effects,  physiopathology
Female
Forearm / blood supply
Humans
Hypertension / drug therapy*,  physiopathology*
Male
Middle Aged
Nifedipine / pharmacology*,  therapeutic use
Vasodilation / drug effects*
Vasodilator Agents / pharmacology*,  therapeutic use
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Calcium Channel Blockers; 0/Vasodilator Agents; 21829-25-4/Nifedipine; 62571-86-2/Captopril

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