Author: Naline E. Bardou M. devillier P. Molimard M. Dumas M. Chalon P. Manara L. Advenier C.
Publisher: Academic Press
ISSN: 1094-5539
Source: Pulmonary Pharmacology & Therapeutics, Vol.13, Iss.4, 2000-08, pp. : 167-174
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Abstract
In the human isolated bronchus (HIB) it has been shown that &bgr;3-adrenoceptor stimulation fails to induce relaxation of airway smooth muscle. It has however been reported in human ventricular endomyocardial biopsies that &bgr;3-adrenoceptor stimulation induced a marked negative inotropic effect which could be linked to Gi protein activation. The aims of this study were: (1) to determine in HIB (internal diameter 1–2 mm) whether the selective &bgr;3-adrenoceptor agonist SR 59119A (N[7-methoxy-1,2,3,4-tetrahydronaphthalen-(2R)methyl]-(2R)-2-hydroxy-2-(3-chloro phenyl)ethanamine hydrochloride) was able to inhibit adenylate–cyclase-mediated airway smooth muscle relaxation induced by isoprenaline, forskolin or vasoactive intestinal peptide (VIP) and (2) to investigate the role of the Gi protein in this interaction. SR 59119A (0.1 μM and 1 μM) induced a shift to the right of concentration response curve for isoprenaline (-0.15±0.06 and -0.54±0.21 log unit,
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