Is there any Evidence of β1-Adrenoceptors Mediating Relaxation of Guinea-pig Lung Parenchyma?

Abstract

Functional evidence was sought for the existence of .beta.1- and .beta.2-adrenoceptors in the isolated guinea-pig parenchymal strip preparation, using potent and selective .beta.1- and .beta.2-adrenoceptor stimulation. To obtain potent .beta.1-adrenoceptor stimulation the nonselective .beta.-adrenoceptor agonist isoprenaline was combined with a highly selective .beta.2-adrenoceptor antagonist ICI 118.551 [erythro-DL-1-(7-methylindan-4-yloxy)-3-isopropylamino-butan-2-ol]. Potent .beta.2-adrenoceptor stimulation was obtained by procaterol. Practolol (.beta.1-adrenoceptor antagonist) and ICI 118,551 were used as antagonists. ICI 118,551, 10-7 mol/l, shifted the concentration response (C/R) curve of isoprenaline to a higher concentration range. The C/R curve of procaterol was shifted in the same way and to the same degree by this concentration of ICI 118,551. The C/R curve of isoprenaline was not further shifted after blockade with a combination of ICI 118,551, 10-7 mol/l, and practolol, 10-6 mol/l. In the trachea preparation, a tissue containing both .beta.1- and .beta.2-adrenoceptors, there was a further shift of the C/R curve of isoprenaline to a higher concentration range after blockade with a combination of ICI 118,551 and practolol in the concentrations given above. In this preparation the shift of the C/R curve of procaterol was 10 times greater than that of isoprenaline after blockade with ICI 118,551, 10-7 mol/l. It is evidently possible to characterize small fractions of .beta.1-adrenoceptors coexisting with .beta.2-adrenoceptors with the technique used. There is still no functional evidence of the existence of .beta.1-adrenoceptors in the lung parenchyma.