Pulmonary function was measured serially in two separate randomized trials of
pindolol in the treatment of
essential hypertension. Patients with overt obstructive airways disease were excluded. In study 1, 131 hypertensive patients were randomized to placebo (31) and 15 mg (33), 30 mg (33), and 60 mg (34) of
pindolol. Pulmonary function was measured before and at weeks 8 and 15 of active medication.
Bronchospasm--a 20% increase in forced expiratory volume in 1 second (FEV1) after
isoprenaline--developed in three patients on active treatment and one on placebo. In eight patients on
pindolol and one on placebo,
bronchospasm ceased. Compared to placebo, no deterioration in pulmonary function occurred with
pindolol and in three tests--maximum voluntary ventilation (MVV) (L/min), MVV%, midexpiratory flow rate (MEFR) (L/min)--significant improvement occurred. In study 2, 14 hypertensive patients were randomized to
pindolol (mean dose 50 mg/day), 15 to
propranolol (mean 360 mg/day), and 14 to
chlorthalidone (mean 107 mg/day). Pulmonary function was measured after 3 weeks of placebo and again after 6 weeks of active treatment. While
propranolol produced slight deterioration in pulmonary function,
pindolol and
chlorthalidone produced slight but significant improvement (p less than 0.05) with maximum MEFR (L/sec). Pulmonary function tests measured after
isoprenaline were significantly worse in patients on
propranolol compared to those on placebo, but were unchanged in patients on
pindolol or
chlorthalidone. The conclusions are: (1)
Pindolol in
antihypertensive doses does not produce airways obstruction and some improvement in pulmonary function may occur. (2) In comparable doses,
pindolol has a positive effect on pulmonary function and
propranolol a negative effect which, when summated, is statistically significant. (3)
Propranolol, but not
pindolol, appears to block the
bronchodilator effects of
isoprenaline. The lack of pulmonary function impairment may be due to intrinsic
sympathomimetic activity properties of
pindolol.