Prohypertensive effects of non-steroidal anti-inflammatory drugs are mostly due to vasoconstriction.

Non-steroidal anti-inflammatory drugs (NSAIDs) have prohypertensive effects and blunt the effects of many antihypertensives. The mechanism of this interaction is still not understood enough. The objective of this investigation was to determine the level of prohypertensive effects of two NSAIDs (ibuprofen, piroxicam) and paracetamol, co-prescribed with two antihypertensive drugs (lisinopril + hydrochlorothiazide, amlodipine), and to improve the understanding of this interaction. A prospective clinical trial, conducted in a Croatian family practice, included 110 already treated hypertensive patients, aged 56-85 years; 50 control patients and 60 patients who were also taking NSAIDs for osteoarthritis treatment. The antihypertensive regimens remained the same during this study, while NSAIDs and paracetamol were crossed-over in three monthly periods. Blood pressure, body weight, serum creatinine, potassium, sodium, diuresis and 24 h urinary sodium excretion were followed-up. In the lisinopril/hydrochlorothiazide subgroup, both ibuprofen and piroxicam elevated mean arterial pressure by 8.9-9.5% (p < 0.001). Body weight increased significantly in the lisinopril/ hydrochlorothiazide + piroxicam subgroup only, while creatinine, urinary output and electrolyte values did not change appreciably in any of the subgroups. NSAID's prohypertensive effects seem to be mostly due to vasoconstriction and, to a minor degree, to volume expansion, since no marked changes in body weight, urinary output, serum creatinine or serum/urinary electrolyte profile were observed.