# COX-2-remming en bloeddrukrespons: graad van remming is bepalend

*geplaatst 2026-02-01 · Hypertensie · Hypertension (Dallas, Tex. : 1979) · doi 10.1161/HYPERTENSIONAHA.124.25516 · https://hartvaat.nl/2026/02/01/cox-2-remming-en-bloeddrukrespons-graad-van-remming-is-bepalend/*

Studie toonde dat de mate van COX-2-remming de bloeddrukrespons moduleert. Selectievere COX-2-remmers geven meer bloeddrukstijging, wat het NSAID-voorschrijfbeleid bij hypertensie informeert.

## English: Degree of Cyclooxygenase-2 Inhibition Modulates Blood Pressure Response.

This study showed that the degree of COX-2 inhibition modulates blood pressure response, with more selective COX-2 inhibitors causing greater blood pressure elevation, informing NSAID selection in hypertensive patients.

## Abstract (original, from the publication)

BACKGROUND: Large clinical trials compared distinct nonsteroidal anti-inflammatory drugs in terms of their risk of adverse cardiovascular events. However, whether pharmacologically equipotent doses were used, that is, whether a similar degree of COX (cyclooxygenase)-2 inhibition was achieved, was not considered. We compared drug target inhibition and blood pressure (BP) response to celecoxib and naproxen. METHODS: Sixteen healthy participants were treated with celecoxib (200 mg/d), naproxen (500 mg/d), or placebo for 7 days in a double-blind, crossover design. The degree of COX inhibition was assessed ex vivo using established whole blood assays and in vivo by quantifying urinary metabolites of thromboxane A2 (COX-1) and prostacyclin (COX-2). Ambulatory BP was measured throughout the final dosing interval. RESULTS: Both nonsteroidal anti-inflammatory drugs inhibited COX-2 activity relative to placebo, but naproxen inhibited COX-2 activity to a greater degree (62.9±21.7%) than celecoxib (35.7±25.2%; P<0.05). Similarly, naproxen treatment inhibited prostacyclin formation in vivo (48.0±24.9%) to a greater degree than celecoxib (26.7±24.6%; P<0.05). Naproxen significantly increased BP compared with celecoxib (mean arterial pressure, +2.5 [95% CI, 1.5-3.5] mm Hg; systolic BP, +4.0 [95% CI, 2.9-5.1] mm Hg; and diastolic BP, +1.8 [95% CI, 0.8-2.8] mm Hg; P<0.05 for all). The difference in systolic BP relative to placebo was associated with the degree of COX-2 inhibition (P<0.05). CONCLUSIONS: Future studies should consider pharmacokinetic and pharmacodynamic properties, as well as patient-specific factors that may modulate the cardiovascular risk of nonsteroidal anti-inflammatory drug use. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02502006.

Auteurs: Katherine N Theken, Soumita Ghosh, Carsten Skarke, Susanne Fries, Nicholas F Lahens, Dimitra Sarantopoulou, Gregory R Grant, Garret A FitzGerald, Tilo Grosser

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Bron: Hypertension (Dallas, Tex. : 1979), https://doi.org/10.1161/HYPERTENSIONAHA.124.25516. Bijgewerkt 2026-07-03T13:31:08Z. Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.