Autoradiographic localization of β‐adrenoceptors in pig lung using [¹²⁵I]‐iodocyanopindolol

Abstract

1 The binding of the P-adrenoceptor radioligand [1251-iodocyanopindolol (I-CYP) antagonists ((± )-propranolol > ICI-1 18551 > atenolol), indicating a predominance of P2-adrenoceptors. Further analysis showed that displacement data for the p1-selective antagonist atenolol and the P2-,selective antagonist ICI-1 18551 were fitted best to a 2 binding site model and that both PI-and Radrenoceptors were present in pig lung in the ratio 28:72 respectively. 4 Autoradiographic grains were localized over tissue and were most dense over alveolar walls > vascular endothelium > vascular smooth muscle > bronchial smooth muscle = bronchial epithelium. Atenolol (10-5M) caused a 31% reduction in specific grain density over alveolar wall tissue, while a 10 fold lower concentration of ICI-l 18551 (10-6M) caused a 50% decrease. These results are consistent with binding data in pig lung parenchyma demonstrating a mixed population of P-adrenoceptors with a predominance of the P2 subtype.5 Approximately 95% of the parenchymal P-adrenoceptors were associated with the alveolar wall as a mixed population of the PI and P2 subtypes in the ratio 30:70 respectively. A greater proportion of the P-adrenoceptors associated with bronchial and vascular smooth muscle seemed to be ofthe 2 subtype. 6 It is possible that the previously described relaxant responses of the pig lung parenchyma strip to Pagonists, mediated via P2-adrenoceptors, resulted from the sum of reactivities in airway and vascular smooth muscle together with relaxation of alveolar interstitial cells.

Postnatal changes in β‐adrenoceptors in the lung and the effect of hypoxia induced pulmonary hypertension of the newborn

“…As in the present study previous reports documented the presence of both βAR subtypes in the porcine lung (Goldie et al ., 1986; McNeel & Mersmann, 1999), and also in the human adult lung parenchyma (Mak et al ., 1996a). We carried out an autoradiographic study in order to locate the receptors and to determine whether the density or type of βAR varied in the different structures.…”

Distribution of β1‐ and β2‐adrenoceptors in mouse trachea and lung: a quantitative autoradiographic study

“…The (Spina et al, 1989a,b), pig (Goldie et al, 1986b) and guinea-pig (Goldie et al, 1986a,c (Henry & Goldie, 1989). Functional studies with mouse isolated trachea also demonstrated a very minor role with respect to tracheal relaxation, for the smaller population (31%) of f2-adrenoceptors (Henry & Goldie, 1989).…”

“…Furthermore, identification of the cellular locations of the P-adrenoceptor subtypes is now possible by the use of autoradiography. High numbers of fi-adrenoceptors have been detected in guinea-pig trachea (Goldie et al, 1986a,c) and human bronchus (Spina et al, 1989a,b), as well as in lung parenchyma from several species, by light microscopic autoradiography (Barnes et al, 1982a;Finkel et al, 1984;Carstairs et al, 1985;Goldie et al, 1986b;Spina et al, 1989a), Author for correspondence. although mouse trachea and lung parenchyma have not previously been studied. In general, these studies have shown that the greatest densities of f-adrenoceptors are found in alveolar septae.…”

“…In general, these studies have shown that the greatest densities of f-adrenoceptors are found in alveolar septae. Studies using this approach have proposed the coexistence of fi1-and fi2-adrenoceptors in alveolar wall and submucosal glands (Carstairs et al, 1985;Goldie et al, 1986b).…”

Equine recurrent airway obstruction does not alter airway muscarinic acetylcholine receptor expression and subtype distribution

“…Already Szentivanyi (1968) hypothesized that the function of the β ‐AR system is impaired and might constitute a potential cause of increased airway smooth muscle sensitivity in asthma. Moreover, impaired β ‐AR responsiveness has been shown in cholinergically stimulated airway smooth muscle from severe asthmatic patients (Goldie et al. , 1986; Bai, 1991; Bai et al.…”