Alterations in surface substructure and degranulation of subapical cytoplasmic granules by mezereinu (MZ) in toad urinary bladder epithelia

Abstract

The increase in transepithelial water flow induced by antidiuretic hormone (ADH) occurs through the ADH V2 receptor, and includes the stimulation of adenylcyclase, an increase in cAMP synthesis and the activation of protein kinase A. These biochemical events in amphibian urinary bladder tissues are reported to be accompanied by apical membrane transformations including the induction of numerous microvilli, and an increase in apical surface area as a result of incorporation of water channels. Amphibian epithelia also contain an ADH V1 receptor coupled to phosphoinositide metabolism and inositol phosphate release. Recently, it was demonstrated that mezerein (MZ), a non-phorbol activator of protein kinase C (PKC)increased transepithelial water flow when added to mucosal surface. The magnitude of water transport was less and occurred over a longer period of time than compared to ADH-stimulated tissues (7,and also Table 1). However, there is little or no information available on ultrastructural studies linking the events due to the ADH V1 receptor and osmotic water flow. Presently, we report on morphological and cytological observations which suggests that the ADH V1 receptor cascade may play a role in the insertion of water channels into the apical membrane possibly through the activation of PKC. The present study utilizes mezerein (MZ), a non-phorbol activator of protein kinase C (PKC) to examine the effect of MZ on epithelial cytomorphology.