Response Of Toad Urinary Bladder Research Articles

Ca2+- and H+-dependent effects of crude bacterial phospholipase C on the hydroosmotic response of toad urinary bladder to serosal hypertonicity.

Phospholipase C (EC 3.1.4.3.) from Clostridium perfringens (crude extracts) was used to study the role of phospholipids in the osmotic permeability of the urinary bladder of the toad. When added to the serosal bath (430 mU/ml) it inhibited the effects of antidiurectic hormone (ADH) and exogenous cyclic AMP. Under the same conditions the increase in osmotic flow produced by serosal hypertonicity (SH) was slightly enhanced by the lipase. The hydroosmotic effect of SH was greatly potentiated by the lipase by decreasing 10-fold the Ca2+ concentration. The SH-induced flow was inhibited by the lipase if the Ca2+ or the H+ concentration was increased 10-fold, but not if the increase in positive charges was produced by a concentration of Mg2+. Phospholipase C had no effect on the action of either ADH or SH if added to the mucosal bath. Serosal neuraminidase or phospholipase A2 could not mimic the effect of phospholipase C on SH. The effect of phospholipase C on the response to SH was not modified if fatty acid-free bovine serum albumin was added to the bath. Therefore, the release of products of lipolysis into the bath do not seem to be responsible for the effects of phospholipase C on SH-induced water flow. The results suggest that the effects of the enzyme on the composition and rearrangement of lipids at the basolateral membrane produce modifications of the water flow. Ca2+ and H+ may modify the enzyme-substrate interaction, suggesting that different phospholipids may be differentially involved in the control of water permeability of the basolateral membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Structural and functional response of toad urinary bladder to LiCl

AbstractStructural and functional response of toad urinary bladder to LiCl. The physiological and morphological response of toad urinary bladder was examined during mucosal exposure of LiCl both with and without vasopressin (VP). With 20 or 100 mU/ml of VP in the serosal bath there was a decrease in Jv between the first and second VP stimulation in LiCl-treated bladders (VP20, -14 ± 6%; VP100, -16 ± 5%) that was not different from that observed without LiCl (VP20, -8 ± 3%, P = NS). However, with 1 mU/ml of VP, a significant decrease in Jv was evident in LiCl-treated (-30 ± 10%) versus control sacs (+6 ± 8%; P < 0.02). At all VP concentrations tested, a significant decrease in SCC and PD was observed between the first stimulation without LiCl and the second stimulation with LiCl. Both osmotic (Pf) and diffusional water permeability (Pd) were increased significantly with 11 mM LiCl only, while neither basal nor VP-stimulated urea permeability (Pu) was affected. Morphological changes paralleled the physiological alterations induced by LiCl. These data demonstrate that LiCl interferes with the osmotic response of the toad bladder to low concentrations of VP, and increases both Pf and Pd while leaving Pu unaffected. These findings coupled with the cell swelling and intracellular vacuolization suggest the presence of a defect in transepithelial water movement somewhere beyond the apical membrane of the granular cell exposed to LiCl.Réponse structurelle et fonctionnelle de la vessie de crapaud au LiCl. La réponse physiologique et morphologique de la vessie de crapaud a été examinée pendant exposition de la muqueuse à du LiCl en présence ou en l'absence de vasopressine (VP). Pour 20 ou 100 mU/ml de VP dans le bain séreux, il y avait une diminution de Jv entre la première et la seconde stimulation par VP dans les vessies traitées par le LiCl (VP20, -14 ± 6%; VP100, -16 ± 5%), qui n'étaient pas différentes de celles observées sans LiCl (VP20, -8 ± 3%; P = NS). Cependant, avec 1 mU/ml de VP, une diminution significative de Jv était évidente dans les sacs traités au LiCl (-30 ± 10%) par rapport aux sacs contrôles (+6 ± 8%; P < 0,02). Pour toutes les concentrations de VP testées, une diminution significative du SCC et de PD a été observée entre la première stimulation sans LiCl, et la seconde stimulation avec LiCl. Les perméabilités osmotiques (Pf) et diffusionnelles (Pd) à l'eau étaient augmentées significativement avec 11 mM de LiCl seulement tandis que la perméabilité à l'urée basale ou stimulée par la VP (Pu) n'était pas affectée. Des modifications morphologiques allaient de pair avec les altérations physiologiques induites par le LiCl. Ces données démontrent que LiCl interfère avec la réponse osmotique de la vessie de crapaud pour de faibles concentrations de VP, augmente Pf et Pd, mais laisse Pu inchangé. Ces résultats, couplés avec le gonflement cellulaire et la vacuolisation intracellulaire suggèrent la présence d'un défaut du mouvement transépithélial d'eau quelque part au delà de la membrane apicale de la cellule granulaire exposée au LiCl.