Subsensitivity to epinephrine following the administration of epinephrine and ephedrine to normal individuals

Pathogenesis of Asthma: A Review

“…Early studies showed that metabolic and cardiovascular responses to {J-agonists were indeed reduced in asthmatic subjects (Cookson & Reed 1963, Middleton & Fink 1968, Logsdon et al 1972, and direct binding studies showed a reduced density of p-receptors on circulating lymphocytes of asthmatics (Brooks et al 1979). However, similar reductions in p-adrenergic responses and {J-receptor density were produced in both normal and asthmatic subjects by administration of p-agonists (Nelson et al 1975, Jenne et al 1977, Conolly & Greenacre 1976, Galant et al 1980, suggesting that the impaired p-adrenergic responsiveness in asthmatic subjects may be explained by tachyphylaxis as a result of prior adrenergic bronchodilator therapy. However, there are some reports of a small impairment in {Jadrenergic responsiveness in asthmatics who have not been treated, or in whom treatment has been withdrawn for over four weeks (Apold & Aksnes 1977.…”

Some alterations of the leucoeyte β2‐adrenoceptor/cAMP‐system in patients with seasonal allergic rhinoconjunctivitis are related to disease activity

“…Many investigations also concentrated, with contradictory results, just on the number of /3-adrcnoceptors (/3adrenoceptor density [12,13]), determined by a so called 'Scatchard analysis', an improper methodology for the determination of /3-adrenoceptors expressed on peripheral blood leucocytes [14][15][16]. In addition, it was often difficult to determine clearly whether the demonstrated abnormalities were caused by medication of the patients studied [5,17]: asthmatics are usually treated with a variety of bronchodilating and anti-inflammatory agents [5], patients with atopic dermatitis often receive topical steroid treatment |iO|, and patients with allergic rhinitis are treated with antihistamines {H|-hlockers).…”