Ultrastructural changes in rat parotid acinar cells after selective beta 1-adrenoceptor agonist treatment.
Administration of the selective beta 1-adrenoceptor agonist, prenalterol, affects the acinar cell of the rat parotid in a manner similar to that observed after isoprenaline (IPR) treatment. Sixty minutes after injection of prenalterol, many cells are depleted of their zymogen granules and there is evidence of secretory protein resynthesis. Long term treatment leads to cellular hypertrophy and marked structural changes in the granule population. The cellular alterations are, however, not as pronounced as those observed after IPR injections. This may be due to the combined beta 1- and beta 2-adrenoceptor effect of IPR. With prenalterol, cell damage is obvious in acute experiments. In long term treated animals numerous characteristic autophagic vacuoles are observed, reflecting a reorganization of cytoplasmic components in superstimulated glands. Although prenalterol and IPR give rise to rather similar structural changes in parotid glands, marked differences between effects of the two drugs on gland biochemistry have been noted. It seems evident that different biochemical pathways involved in secretory activity have actions in common with respect to effects on submicroscopical structures.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D007545:Isoproterenol / Q000494:pharmacology; D008854:Microscopy, Electron; D010306:Parotid Gland / Q000187:drug effects / Q000648:ultrastructure*; D011217:Practolol / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology; D011294:Prenalterol; D051381:Rats; D011919:Rats, Inbred Strains
D000318:Adrenergic beta-Agonists; D007545:Isoproterenol; D011294:Prenalterol; D011217:Practolol