Numerous studies have been, and are being devoted to the nature of
adrenergic and
purinergic receptors in the bronchopulmonary system. Studies of beta-
adrenoceptors performed with
ligands (table I) have demonstrated the presence of two types of receptors, beta 1 and beta 2 in proportions of about 15 : 100 respectively; this proportion is approximately the same at all levels of the tracheobronchial tree. Beta-
adrenoceptors (beta 1 + beta 2) are globally more numerous in peripheral organs which contain heterogeneous tissues. Their number can be modified in certain circumstances, notably in
asthma,
infection and after prolonged treatment with
sympathomimetic amines. Functional studies using specific beta 1-adrenoceptor agonists (
RO-363 or
prenalterol) or determining the relative activities of beta 1 and/or beta 2 stimulants and their inhibition by selective beta-blockers have shown that stimulation of beta 1-adrenoceptors may produce partial relaxation of the isolated trachea but not of lung parenchyma, the latter being supposed to represent distal airways. Studies on isolated small bronchi, about 0.1 mm in diameter (fig. 1 and 2A) have confirmed that stimulation of beta 1-adrenoceptors has not effect on distal airways. They have also demonstrated that beta 2-stimulants have different intrinsic activities (fig. 2B). Studies of
alpha-adrenergic receptors using
ligands (table II) have shown that these receptors are in small number in the tracheobronchial tree of numerous animal species. Functional studies on the conscious guinea-pig have shown that
clonidine can potentiate the
bronchoconstrictor effects of
acetylcholine,
histamine and
serotonin (fig. 3) and that this potentiating effect is specifically inhibited by
yohimbine and
piperoxan (fig. 4). This action of
clonidine has been attributed to depression of the reflex sympathetic activity associated with
bronchospasm. Alpha 1-adrenoceptor agonists (
phenylephrine,
methoxamine) induce
contracture of the isolated bronchial smooth muscle (fig. 5) but may partially reduce the
bronchoconstrictor effects of
acetylcholine,
histamine or
serotonin (fig. 6). This last effect is partially inhibited by alpha 1-blockers (fig. 7) and seems to be due to shrinkage of the bronchial mucosa. Finally, studies of
purinergic receptors in the bronchopulmonary system have shown that they probably are of the A2-P1 type (tables III and IV) and that they do not seem to be involved in the
bronchodilator activity of
theophylline.