Selectivity of clenbuterol (NAB 365) in guinea-pig isolated tissues containing beta-adrenoceptors.
The effects of clenbuterol (ANB 365), an aminohalogen substituted phenylethanolamine, have been examined on isolated tissue preparations from guinea-pigs. Clenbuterol produced concentration (or dose)-dependent relaxations of tracheal chains, decreases in perfusion pressure of hind limb blood vessels, inhibitions of acetylcholine-induced contractions of the uterus, increases in atrial rate and inhibitions of electrically-induced contractions of the ileum. These responses were blocked by propranolol. Clenbuterol was similar in potency to isoprenaline on the trachea (carbachol-contracted), hind limb and uterus (beta2-adrenoceptors) but was significantly less potent than isoprenaline on the atria and the ileum (beta1-adrenoceptors). Clenbuterol produced marked relaxation of intrinsic tone tracheal preparations in concentrations up to 3000 times less than were required on carbachol-contracted preparations, whereas for isoprenaline the concentrations required on intrinsic tone preparations were only 55 fold less. It is concluded that clenbuterol is a beta-adrenoceptor agonist and that it is a partial agonist on the carbachol-stimulated trachea, on the atria and on hind limb blood vessels. It shows beta2-selectivity in that its potency, relative to that of isoprenaline, on the preparations containing beta2-adrenoceptors was much higher than on those with beta1-adrenoceptors. On intrinsic tone tracheal preparations it may produce an additional relaxant effect responsible for its high potency on that preparation.
Selectivity of clenbuterol (NAB 365) in guinea-pig isolated tissues containing beta-adrenoceptors. The effects of clenbuterol (ANB 365), an aminohalogen substituted phenylethanolamine, have been examined on isolated tissue preparations from guinea-pigs. Clenbuterol produced concentration (or dose)-dependent relaxations of tracheal chains, decreases in perfusion pressure of hind limb blood vessels, inhibitions of acetylcholine-induced contractions of the uterus, increases in atrial rate and inhibitions of electrically-induced contractions of the ileum. These responses were blocked by propranolol. Clenbuterol was similar in potency to isoprenaline on the trachea (carbachol-contracted), hind limb and uterus (beta2-adrenoceptors) but was significantly less potent than isoprenaline on the atria and the ileum (beta1-adrenoceptors). Clenbuterol produced marked relaxation of intrinsic tone tracheal preparations in concentrations up to 3000 times less than were required on carbachol-contracted preparations, whereas for isoprenaline the concentrations required on intrinsic tone preparations were only 55 fold less. It is concluded that clenbuterol is a beta-adrenoceptor agonist and that it is a partial agonist on the carbachol-stimulated trachea, on the atria and on hind limb blood vessels. It shows beta2-selectivity in that its potency, relative to that of isoprenaline, on the preparations containing beta2-adrenoceptors was much higher than on those with beta1-adrenoceptors. On intrinsic tone tracheal preparations it may produce an additional relaxant effect responsible for its high potency on that preparation.