In this study on a small group of selected patients Adth coexisting hypertension and asthma, a singledose challenge with atenolol, 100 mg, caused bron-choconstriction in most subjects, while the response to single-dose challenge with celiprolol, 400 mg, closely resembled that with placebo. Without the sustained bronchodilator benefit of beta-2 agonists during the preceding 10-h period, the adverse effect of atenolol on FEVi, FVC and PEF was obvious. canadian health&care mall
Following salbutamol inhalation, respiratory parameters improved to prechallenge levels (p<0.05), suggesting that atenolol, 100 mg, is sufficiently cardio-selective to preserve a clinical bronchial responsiveness to beta-2 agonists.
Similarly, after celiprolol, bronchial responsiveness to the salbutamol was retained. The fact that further bronchodilation could be achieved by salbutamol suggests that any intrinsic sympathomimetic activity on the bronchial tree is minor compared with salbutamol. Pruss et al have suggested that the bronchodilatory effect of celiprolol is not due to beta-2 ISA, since it is unaffected by pretreatment with propranolol in the cat model. Other beta-blockers possessing ISA, such as oxprenolol, acebutolol and pindolol, have not shown bronchosparing properties in single-dose studies. Celiprolol did not cause any bradycardia, which may be explained by its peripheral vasodilatory properties, although beta-1 agonist effects cannot be excluded.
Both atenolol and celiprolol were modestly effective antihypertensive agents and approximately half of the patients achieved the goal diastolic blood pressure with either agent. The optimal antihypertensive dose for each of these patients might not have been given, although the doses chosen are of established antihypertensive potency.