Open AccessHypertrophy and Dysfunction of Parotid Gland Induced by Chronic Stimulation of β1-Adrenergic Receptors
Author(s) -
Yuko Suzuki,
Hideyo Ohshika
Publication year - 1985
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.39.419
Subject(s) - stimulation , muscle hypertrophy , parotid gland , adrenergic , adrenergic receptor , medicine , receptor , endocrinology , pathology
The present study was carried out to determine the beta-receptor subtype responsible for the hypertrophy and dysfunction of parotid glands in rats chronically treated with isoproterenol (ISP). Treatment with dobutamine (DBT), a beta 1-agonist, (30 mg/kg twice a day for 4 days) produced a significant enlargement of the parotid gland just as in the ISP-treated rats. The effects of secretagogues on amylase release and ISP-induced cyclic AMP accumulation were markedly decreased in the parotid tissue of the treated rats. Co-administration of the beta 1-antagonists metoprolol and acebutolol clearly inhibited the development of parotid enlargement and its secretory dysfunction induced by ISP or DBT. Procaterol treatment (30 mg/kg, twice a day for 4 days) did not cause any dysfunction or any increase in the gland weights. These results indicate that both hypertrophy and dysfunction of the rat parotid gland, which were observed in chronic treatment with ISP, may result from chronic stimulation of beta 1-adrenoceptors.