Clinical and experimental hypertension. Part A, Theory and practice · 1984
Effects of indomethacin, sulindac, naproxen, aspirin, and paracetamol in treated hypertensive patients.
Клиническое исследованиеСравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chalmers J P, West M J, Wing L M, Bune A J, Graham J R
Аннотация
Four placebo controlled, randomised crossover studies were carried out to investigate the effects of non-steroidal anti-inflammatory drugs and analgesics on blood pressure control in treated hypertensive patients. Twelve patients completed one study comparing indomethacin, 25 mg tds, with placebo in 2 six week phases; there were increases in mean blood pressure (p less than 0.01) of 9 mm Hg (casual), 8 mm Hg (supine) and 10 mm Hg (standing) in the indomethacin phase accompanied by a 50% reduction in plasma renin activity (p less than 0.05) and a 47% decrease in plasma aldosterone concentration (p less than 0.05). Similar studies on aspirin-SR, 650 mg daily (19 patients), and paracetamol, 1 g 8th hourly (20 patients), revealed only small changes in blood pressure, with a 2 mm Hg increase in supine diastolic blood pressure during aspirin therapy and a 4 mm Hg increase in supine and standing systolic blood pressure during paracetamol therapy (p less than 0.05 for both). Nineteen patients completed a study with 4 three week phases, taking placebo, naproxen 250 mg mane and 500 mg nocte, sulindac 200 mg bd, and aspirin-SR 1950 mg bd. All three active agents depressed plasma renin activity and plasma aldosterone concentration. Neither sulindac nor aspirin caused any significant increases in blood pressure, and naproxen had little effect, though it did cause a 4 mm Hg increase in standing systolic pressure (p less than 0.05). We conclude that the effects of indomethacin on control of blood pressure in treated hypertensive patients are not exhibited to the same extent by other drugs investigated, and that they are not dependent on the concomitant decreases in plasma renin activity or plasma aldosterone concentration. The importance of inhibition of prostaglandin synthesis remains unclear.