Comparison of ketanserin and slow‐release nifedipine added to the treatment of hypertensive patients uncontrolled by a thiazide diuretic plus beta‐adrenoceptor blocker.

Abstract

1 Ketanserin or slow-release nifedipine were added to the treatment of 24 patients with hypertension uncontrolled by a thiazide diuretic plus 13-adrenoceptor antagonist in an observer-blind, randomised parallel-group study of 6 months duration. 2 At 6 months the mean falls in supine blood pressure were for ketanserin (mean daily dose 77 mg) 7/5 mm Hg and for nifedipine (mean daily dose 62 mg) 27/10 mm Hg. The difference between the treatments was significant for systolic blood pressure (P < 0.02) and mean arterial pressure (P < 0.05). Six nifedipine-treated patients reached target blood pressure, compared with one patient with ketanserin (P < 0.02). 3 One patient taking nifedipine, and nonetaking ketanserin withdrew because of sideeffects. The tolerability of the two drugs was broadly similar. 4 Ketanserin treatment was associated with significant changes in supine pulse rate (-8 beats min-', P < 0.05) and corrected QT interval (+27 ms, P < 0.05). Nifedipine treatment had no effect on these variables. The change in pulse rate was significantly different between the groups. 5 In patients treated with a diuretic and ,3-adrenoceptor blocker who required additional treatment ketanserin was significantly inferior to nifedipine.

Effects of short‐term ketanserin treatment on the QT interval and vagal function in healthy subjects

“…In vivo, ketanserin causes prolongation of the QT, interval, consistent with Class I11 antiarrhythmic activity (Waller, Solomon & Ramsay, 1987;Donnelly, Elliot, Meridith & Reid, 1987). Ketanserin may also modify reflex control of heart rate, as indicated by the absence of an appropriate increase in heart rate in response to the decrease in blood pressure caused either by acute or chronic drug administration (Fagard et al, 1984;Zabludowski, Zoccali, Isles, Murray, Robertson, Inglis, Fraser & Ball, 1984). Ketanserin may also modify reflex control of heart rate, as indicated by the absence of an appropriate increase in heart rate in response to the decrease in blood pressure caused either by acute or chronic drug administration (Fagard et al, 1984;Zabludowski, Zoccali, Isles, Murray, Robertson, Inglis, Fraser & Ball, 1984).…”