ECL cells involvement in the isoproterenol-induced gastroprotection. An ultrastructural study.

The central and peripheral adrenergic systems are involved in the regulation of several functions in the gut including the maintenance of gastric microcirculation and gastric secretion but little is known about the role of the adrenergic system, in particular, beta-adrenoceptors in the phenomenon of gastroprotection. In this study acute gastric lesions were provoked by an intragastric (i.g.) application of 100% ethanol in rats with topical application of isoproterenol (ISO) (1 mg/kg) or subcutaneous (s.c.) administration of ranitidine (RAN) (40 mg/kg) or both. An area of gastric lesions was determined by planimetry, gastric blood flow (GBF) was determined by H2-gas clearance technique and gastric specimens were taken for histology and electron microscopy. It was found that ISO reduced ethanol-induced gastric mucosal lesions and this effect was accompanied by a rise in GBF. In contrast, RAN applied s.c. in a dose that produced almost complete achlorhydria, failed to affect ethanol-lesions but attenuated significantly ISO induced gastroprotection and abolished the increase in the GBF induced by this beta-adrenoceptor agonist. Histology and ultrastructural study revealed that pretreatment with ISO influenced HCl production reflected by the elaborated secretory surface of parietal cell intracellular canaliculi. All these changes were accompanied by the ultrastructural changes in Golgi apparatus in ECL-like cells (histamine storing cells). Pretreatment with ISO caused the collapse of Golgi profiles and only peripheral sacs were not compressed but such a change was not observed after RAN treatment. The best developed Golgi was, however, seen in the control rats without any treatment. Secretory granules in ECL cells were significantly expanded after pretreatment with ISO but did not show significant morphological changes in rats pretreated with RAN. We conclude that 1. ISO protects the gastric mucosa injured by ethanol presumably due to increased gastric microcirculation, and 2. ECL-like cells are actively involved in ISO-induced gastroprotection possibly by the increased histamine release which is reflected by ECL-cell and Golgi apparatus morphology.