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Captopril, but not nifedipine, improves endothelium-dependent vasodilation in hypertensive patients

Millgård, Jonas (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
Hägg, Anders (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
Sarabi, M. (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
visa fler...
Lind, Lars (författare)
Uppsala universitet,Institutionen för medicinska vetenskaper
visa färre...
 (creator_code:org_t)
1998
1998
Engelska.
Ingår i: Journal of Human Hypertension. - 0950-9240 .- 1476-5527. ; 12:8, s. 511-516
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
Abstract Ämnesord
Stäng  
  • 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.

Nyckelord

hypertension
blood pressure
endothelium
vasodilation
ACE-inhibitors
calcium-antagonists
MEDICINE
MEDICIN

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Av författaren/redakt...
Millgård, Jonas
Hägg, Anders
Sarabi, M.
Lind, Lars
Artiklar i publikationen
Journal of Human ...
Av lärosätet
Uppsala universitet

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