Comparison of atenolol and oxprenolol in patients with angina or hypertension and co‐existent chronic airways obstruction.

1. The effects of single oral doses of 10 mg bisoprolol and 400 mg acebutolol on respiratory function were studied in nine smokers with airway obstruction in a double‐blind, placebo‐controlled experiment. 2. The effects of the drugs were assessed by measuring specific airway conductance (sGaw) for 3 h after their administration and by studying their interaction with the bronchodilator response to inhaled salbutamol. 3. sGaw did not change for 3 h after bisoprolol or acebutolol administration. The bronchodilator response to inhaled salbutamol was not affected by bisoprolol but significantly reduced by acebutolol (P less than 0.05 vs placebo). 4. Under these conditions, bisoprolol behaves like a selective beta 1‐adrenoceptor antagonist but acebutolol exhibits less beta 1‐adrenoceptor selectivity.

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Comparative effects of bisoprolol and acebutolol in smokers with airway obstruction.

Macquin‐Mavier¹,

Roudot-Thoraval²,

Clérici³

et al. 1988

“…However, compara-tive studies between different cardioselective 1-adrenoceptor blockers in asthmatic patients have shown little differences in their effect on airway calibre (Vilsvik & Schaanning, 1976;Lofdahl & Svedmyr, 1981). In patients with more fixed chronic airflow obstruction, cardioselective drugs have been shown to produce significantly less bronchoconstriction (Perks et al 1978;Sinclair, 1979).…”

Section: Discussionmentioning

confidence: 99%

Assessment of airways, tremor and chronotropic responses to inhaled salbutamol in the quantification of beta 2‐adrenoceptor blockade.

Lipworth

Brown

McDevitt

1989

1 The purpose of the study was to assess and compare the effects of inhaled salbutamol on heart rate (HR), finger tremor (Tr) and specific airways conductance (sGaw) in the measurement of 32-adrenoceptor blockade in normal subjects. 2 Five healthy volunteers were given oral doses of atenolol 50 mg, 100 mg, 200 mg (AS0, A100, A200), propranolol 40 mg (P40) or identical placebo (P1) in a single-blind crossover design. 3 Three hours after drug ingestion, dose-response curves were constructed using cumulative doses of inhaled salbutamol: 200 ,g, 700,ug, 1700 ,ug, 3200 ,ug, 6200,ug. HR, Tr and sGaw were measured at each dose increment, made every 20 min. 4 Increasing doses of atenolol were associated with progressive reduction in salbutamol induced ,-adrenoceptor responses. The greatest attenuation occurred with propranolol. These effects on ,B-adrenoceptor responses were similar for HR, Tr and sGaw. Geometric mean dose ratios (compared with placebo) for AS0, A100, A200 and P40 were as follows HR: 1.98, 2.75, 4.29; Tr: 1.60, 3.78, 6.34, 80.50; sGaw: 1.08, 4.35, 12.30, 66.0 (no dose ratio was obtained for HR with P40). 5 These results showed that atenolol and propranolol attenuated the effects of salbutamol on HR to a similar degree as Tr and sGaw. Furthermore, the variability was least in the measurement of chronotropic responses, suggesting that this may be used to quantify 132-adrenoceptor antagonism. The B1-adrenoceptor selectivity of atenolol was a dosedependent phenomenon, although the 132-adrenoceptor blockade of A200 was much less than with P40.

“…There are, however, differences in the degree of selectivity of the cardioselective ,-adrenoceptor blockers since they displace to varying extents the bronchial dose-response curves to 32-adrenoceptor stimulants. In clinical studies, atenolol or bisoprolol appeared to be more selective than other compounds, such as acebutolol, metoprolol or oxprenolol (Greefhorst & van Herwaarden, 1982;Gribbin et al, 1981;Lammers et al, 1984;Lawrence et al, 1982;Macquin-Mavier et al, 1988;Perks et al, 1978;Ruffin et al, 1979;Tattersfield et al, 1984). Bronchial rings from a segmental bronchus were prepared and suspended in parallel in Krebs solution under an initial tension of 2.5 g. After 1.5 h of equilibration, the resting tension was between 1 and 2 g. Tensions were measured isometrically with strain gauges, amplifiers and .O.S..-Moise 2 recorder system (Celaster, Celle l'Evescault, 86600 Lusignan, France) (Advenier et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Comparative beta‐adrenoceptor blocking effects of propranolol, bisoprolol, atenolol, acebutolol and diacetolol on the human isolated bronchus.

Naline¹,

Sarriá²,

Ertzbischoff³

et al. 1990

Cedex 06 and 2Laboratoires Lederle, 74, rue d'Arcueil, SILIC 275, 94578 Rungis Cedex, France Five P-adrenoceptor blockers, propranolol, acebutolol, diacebutolol, atenolol and bisoprolol, were tested for their antagonistic effect against isoprenaline on human isolated bronchi. The results showed (1) that only propranolol exerted a competitive antagonistic effect against isoprenaline (pA2 = 9.40 ± 0.22, n = 7) whereas the other drugs did not, and (2) that, in the presence of P-adrenoceptor blockers in the plasma concentrations reported after a single usual therapeutic dose, the doses of isoprenaline giving the same bronchodilator effect must be multiplied by 32.6, 5.51, 4.63, 2.82 and 1.95 respectively with propranolol, diacetolol, acebutolol, atenolol, and bisoprolol. It was concluded that (1) atenolol and bisoprolol were the least potent drugs at bronchial level in therapeutic plasma concentrations and (2) that tests performed on the human isolated bronchus might be a useful screening procedure for new drugs with potential activity on the airways.