Cell-Enlargement-Related Polypeptides Are Induced via β1-Adrenoceptors in Mouse Parotids

Abstract

Induction of cell and gland enlargement (growth-in-size) and induction of a group of secretory polypeptides (polypeptides C–G) seem to occur in close relationship in mouse parotid glands stimulated chronically by the nonselective β-adrenergic agonist isoproterenol. To determine whether β1, β2, or both subtypes of β-adrenergic receptors are involved in those responses, dose-dependency studies were carried out during a 7-day period of daily stimulations to assess the relative abilities of the selective β-adrenergic agonists dobutamine (β1) and salbutamol (β2) to induce polypeptides C–G and growth-in-size. The relative abilities of the selective β-adrenoceptor antagonists atenolol (β1) and I.C.I. 118.551 (β2) to interfere with the induction of both responses by chronic treatment with the various β-adrenergic agonists were also studied. Parotid growth-in-size was assessed by evaluating wet weight, whole protein content, and light microscopy histology. The presence of polypeptides C–G was evaluated after SDS–polyacrylamide gel electrophoresis and Coomassie blue staining. Under these experimental conditions, dobutamine was found to be at least one order of magnitude more potent than salbutamol at inducing growth-in-size. Dobutamine was also found to be clearly stronger than salbutamol as an inducer of polypeptides C–G. On the other hand, atenolol was more effective than I.C.I. 118.551 at preventing the induction of polypeptides C–G and growth-in-size by isoproterenol, dobutamine, or salbutamol. Taken together, these results suggest that in mouse parotid glands, polypeptides C–G and growth-in-size are induced preferentially via adrenergic receptors of the β1-subtype.